Uncover the benefits of integrative therapies for cognitive decline in maintaining mental agility and promoting healthy aging.
Dementia, and particularly Alzheimer’s disease (AD), represents one of the most significant and rapidly evolving areas of clinical medicine in the twenty-first century. As our understanding of the underlying biology of Alzheimer’s disease deepens, so too does the complexity of the diagnostic frameworks we use and the treatment strategies we employ. This educational post presents a comprehensive, evidence-based overview of the pharmacological management of dementia, with a primary focus on Alzheimer’s disease, drawing upon the work of leading researchers and clinicians in the field, including the landmark contributions of Dr. Clifford Jack and the teams behind the ATN diagnostic criteria and the evolving disease-modifying therapies (DMTs) now entering clinical practice.
The topics covered in this post include the neurotransmitter dysregulations that underlie the cognitive and neuropsychiatric symptoms of dementia, a structured and clinically grounded approach to prescribing for both cognitive and behavioral symptoms, a detailed exploration of the biological underpinnings of Alzheimer’s pathology including amyloid, tau, and neurodegeneration, the significance of recognizing co-occurring neuropathologies in real-world patients, and the emerging role of biomarker-based diagnosis in guiding treatment decisions for disease-modifying therapies.
Crucially, this post also situates these clinical findings within the broader framework of integrative and multidisciplinary care as practiced at Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas. At this clinic, I work alongside Dr. Maria Guadalupe Cardenas, MD, a board-certified internist with over 40 years of clinical experience, who serves as Medical Director and Collaborative Physician. Together, our team integrates chiropractic care, functional medicine, internal medicine oversight, rehabilitation, and personal injury care into a cohesive, patient-centered treatment model. We believe that the evidence presented in this post reinforces the necessity of this kind of comprehensive, integrative approach when managing complex neurological conditions such as Alzheimer’s disease and related dementias.
Whether you are a clinician, a caregiver, a patient, or simply someone seeking to understand the current landscape of dementia care, this post is designed to take you on a clear, evidence-based, and clinically meaningful journey through one of medicine’s most pressing challenges.
Hello, and welcome. I’m Dr. Alex Jimenez. With my diverse background as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), Family Nurse Practitioner (FNP-BC), Certified Functional Medicine Practitioner (CFMP), and an Institute for Functional Medicine Certified Practitioner (IFMCP), among other specializations, my life’s work has been dedicated to an integrative and holistic approach to health. Today, I want to take you on a journey into one of the most pressing health challenges of our time: cognitive decline.
At our practice, the Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, located in El Paso, Texas, we pride ourselves on a unique, multidisciplinary model of care. A cornerstone of our practice is the collaborative relationship I share with Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933). Dr. Cardenas is a highly respected, board-certified Internist with over four decades of clinical experience. As our Medical Director and Collaborative Physician, she provides invaluable medical oversight, ensuring our patients receive the highest standard of care that bridges conventional medicine with the advanced principles of chiropractic and functional medicine. This integrated setup is not just a matter of convenience; it is a philosophical commitment to treating the whole person. By combining my expertise in musculoskeletal health, neurological function, and systems biology with Dr. Cardenas’s profound knowledge of internal medicine, we can address complex conditions like cognitive decline from multiple angles. Our team approach allows us to manage everything from personal injury and rehabilitation to chronic disease and wellness optimization, always with the patient’s comprehensive well-being at the forefront.
In this educational post, I’m excited to share the latest findings from leading researchers in neurology and dementia care. We’ll be looking at their work through the lens of modern, evidence-based research, and I will weave in my own clinical observations and explain how our integrative chiropractic approach fits into this evolving treatment landscape. This is not a formal lecture but an educational journey designed to be clear, comprehensive, and empowering for both patients and fellow healthcare professionals.
When I engage with patients, families, and colleagues about dementia care, I always begin at the same place: we cannot treat what we have not clearly understood. The journey of managing Alzheimer’s disease and related dementias begins not in the pharmacy, but in the diagnostic workup, in the conversation at the bedside, and in the careful mapping of how a person’s brain is changing and why. This foundational orientation is what separates reactive symptom management from genuinely proactive, precision-informed care.
Dementia is not a single disease. It is a clinical syndrome characterized by a progressive decline in cognitive function severe enough to interfere with a person’s ability to carry out daily activities independently. Within this syndrome, Alzheimer’s disease is by far the most common cause, accounting for approximately 60 to 80 percent of all dementia cases in older adults. However, as we will discuss at length in this post, many individuals with Alzheimer’s disease also carry additional neuropathological burdens simultaneously, meaning that the clinical picture is often considerably more complex than a single diagnosis might suggest.
This complexity matters enormously for treatment. It matters for which medications we choose, for what dose, for how long, and alongside what other interventions. It also matters for how we counsel patients and their care partners, and how we integrate non-pharmacological approaches, including chiropractic, functional medicine, and rehabilitative care that form the backbone of our practice here at Injury Medical Clinic PA in El Paso, Texas.
One of the unique and essential aspects of evaluating cognitive decline is gathering information from a secondary historian. This is someone who knows the patient well—a spouse, a child, a close friend—who can provide an outside perspective. I am careful not to label this person a “caregiver,” as that term can carry a certain weight. Instead, they are a trusted partner in the information-gathering process.
I always explain to my patients that this is a collaborative effort. I emphasize that the information flows to me, the clinician, not from me to the other person. Most of my patients are very receptive to this. We all have blind spots; there are things we do or say that we don’t even recognize, but those closest to us often notice. The secondary historian can provide invaluable insights into changes in behavior, personality, or daily functioning that the patient may be unaware of or unintentionally downplay. This dual perspective is a cornerstone of a robust diagnostic workup.
The traditional model of diagnosing Alzheimer’s disease relied heavily on clinical symptom observation. A clinician would evaluate the nature of a patient’s cognitive complaints, assess which functional domains were impaired, and use the pattern and timing of symptom onset to arrive at a diagnosis of “probable Alzheimer’s disease.” This approach, while clinically useful, was inherently limited. It could only identify the disease after significant neurological damage had already occurred, and it could not definitively distinguish Alzheimer’s disease from other causes of dementia with perfect reliability.
What we now understand, thanks in large part to the pioneering work of researchers such as Dr. Clifford Jack at the Mayo Clinic, is that Alzheimer’s disease is not a condition that begins when symptoms appear. Rather, the biological processes that define Alzheimer’s disease, specifically the abnormal accumulation of the proteins beta-amyloid and tau, begin fifteen to twenty years before any measurable cognitive impairment becomes apparent. This insight, visually captured in what many researchers informally call the “Jack curves,” has transformed how we think about the disease timeline and, critically, when and how we should intervene.
The practical implication is profound: by the time a patient walks into a clinic complaining of memory problems, a significant amount of irreversible neuronal damage has already occurred. This does not mean that diagnosis and treatment are futile at that stage. Still, it does underscore the urgency of developing better tools for earlier identification and the importance of timely, accurate diagnosis when symptoms do appear.
To understand why the treatments we use work as they do and why the disease-modifying therapies emerging in recent years represent such a significant scientific advance, it is essential to grasp the underlying biology of Alzheimer’s disease at a mechanistic level.
Beta-amyloid is a protein fragment that is produced as a natural byproduct of normal brain metabolism. In a healthy brain, beta-amyloid is continuously produced and cleared, maintaining a balance that prevents accumulation. In the Alzheimer’s brain, this balance is disrupted. Beta-amyloid is either overproduced, or its clearance mechanisms are impaired, or both. As a result, the protein begins to accumulate in the brain parenchyma.
Initially, beta-amyloid exists in a soluble form, meaning it circulates as individual molecules or small oligomers. Many researchers consider these soluble oligomers among the most neurotoxic forms of the protein. Over time, however, soluble amyloid aggregates further and eventually form insoluble amyloid plaques, also known as neuritic plaques or senile plaques. These plaques deposit in the spaces between neurons and are one of the hallmark pathological features of Alzheimer’s disease on autopsy or advanced neuroimaging.
The current leading hypothesis, known as the amyloid cascade hypothesis, proposes that beta-amyloid accumulation is the initiating event in the pathological cascade of Alzheimer’s disease. According to this framework, the presence of amyloid in the brain triggers a downstream series of events, including the pathological transformation of tau protein, neuroinflammation, synaptic dysfunction, and ultimately widespread neuronal death.
Tau is a protein that plays a critical structural role in healthy neurons. Its primary function is to stabilize microtubules, which are the structural scaffolding inside neurons that facilitate the transport of nutrients, organelles, and signaling molecules from the cell body to the axon terminals and back. In other words, tau maintains the neuron’s internal transport system.
In Alzheimer’s disease, tau undergoes a process called hyperphosphorylation, in which it becomes abnormally modified by the addition of excessive phosphate groups. This hyperphosphorylated tau can no longer bind microtubules effectively, causing the microtubule network to destabilize and collapse. The rogue tau protein then clumps together with other misfolded tau molecules, eventually forming neurofibrillary tangles inside the neuron. These tangles physically clog the neuron’s internal machinery, disrupt its ability to communicate with other neurons, and ultimately contribute to neuronal death.
Braak staging, a system developed by neuroanatomists Heiko and Eva Braak, provides a standardized framework for measuring the severity and spatial distribution of tau pathology in the brain. The Braak stages range from I through VI, with lower stages representing tau tangles confined to the entorhinal cortex and hippocampus (regions critical for memory formation), and higher stages representing tangles that have spread throughout the neocortex. This is why early Alzheimer’s disease most commonly presents with memory impairment, specifically the inability to encode and retrieve recent memories, since the hippocampus is among the first brain regions to be affected by tau pathology.
One of the most clinically significant insights to emerge from decades of biomarker research is the recognition that the pathological processes of Alzheimer’s disease unfold over an extraordinarily long timeline before any symptoms become clinically apparent. As Dr. Jack’s research has demonstrated, amyloid accumulation begins approximately fifteen to twenty years before the onset of measurable cognitive impairment. Tau pathology follows, and the combination of amyloid and tau together drives the neurodegeneration that eventually crosses the threshold of symptom expression.
This has several important clinical implications that I address directly in my practice at Injury Medical Clinic PA:
For many years, the clinical diagnosis of Alzheimer’s disease was made primarily by ruling out other causes of dementia and identifying a characteristic clinical pattern of symptoms. While this approach has served clinicians reasonably well in the majority of cases, it has well-recognized limitations: it cannot confirm the diagnosis with certainty in a living patient, it cannot detect the disease in its preclinical or prodromal stages, and it cannot always distinguish Alzheimer’s disease from other dementias, particularly in atypical presentations.
The ATN framework, first articulated in a landmark 2011 publication by Dr. Jack and colleagues, and subsequently updated and refined in the years that followed, represents a paradigm shift in how we conceptualize and diagnose Alzheimer’s disease. The ATN framework defines Alzheimer’s disease not by its clinical symptoms, but by its underlying biological signature: the presence of abnormal amyloid (A), abnormal tau (T), and evidence of neurodegeneration (N). Let me walk through each of these components in detail.
The “A” in ATN refers to evidence of amyloid pathology in the brain. Currently, there are several established methods for detecting abnormal amyloid accumulation:
Cerebrospinal Fluid (CSF) Amyloid: A lumbar puncture can be performed to sample the cerebrospinal fluid, which bathes the brain and spinal cord. In Alzheimer’s disease, CSF levels of amyloid-beta 42 (Abeta42) are characteristically reduced, not elevated, because the amyloid is being sequestered in plaques in the brain parenchyma rather than circulating freely in the CSF. This is an FDA-approved and well-validated diagnostic test. However, it requires a skilled clinician to perform the lumbar puncture and carries some procedural discomfort and risk for the patient.
Amyloid PET Imaging: Positron emission tomography (PET) scans using amyloid-specific radiotracers, such as florbetapir, florbetaben, or flutemetamol, allow direct visualization of amyloid plaques in the living brain. A positive amyloid PET scan shows characteristic patterns of radiotracer uptake in brain regions known to be early sites of amyloid deposition, such as the precuneus, posterior cingulate cortex, and frontal cortex. Amyloid PET is FDA-approved and is covered by Medicare under specific circumstances defined by appropriate use criteria.
Blood-Based Amyloid Tests: In recent years, significant progress has been made in developing plasma biomarkers for Alzheimer’s disease. Tests measuring plasma amyloid-beta 42/40 ratio and plasma phosphorylated tau (p-tau) have demonstrated impressive accuracy in identifying individuals with brain amyloid positivity. These tests are far less invasive than CSF collection or PET imaging and considerably more accessible and affordable. However, it is important to note that blood-based amyloid tests are not currently considered the gold standard for diagnosis. They are valuable as screening or triage tools, particularly in primary care settings. Still, a positive blood-based test typically requires confirmation with a more definitive modality before it is used to guide treatment decisions, particularly decisions about disease-modifying therapies.
The “T” in ATN refers to evidence of tau pathology. Like amyloid, tau can be detected through CSF analysis or PET imaging:
CSF Tau: Both total tau (t-tau) and phosphorylated tau (p-tau) can be measured in the CSF. In Alzheimer’s disease, both t-tau and p-tau are typically elevated, reflecting the ongoing production and accumulation of neurofibrillary tangles. Elevated p-tau, in particular, is considered a relatively specific marker for Alzheimer’s pathology, as opposed to other causes of elevated total tau such as acute neuronal injury.
Tau PET Imaging: Just as amyloid-specific radiotracers can image amyloid plaques, tau-specific radiotracers such as flortaucipir (Tauvid) can image neurofibrillary tangles in the brain. Tau PET provides spatial information about the distribution and burden of tau pathology, which correlates well with Braak staging and with the clinical severity of cognitive impairment. Tau PET is FDA-approved and represents an increasingly important tool in the comprehensive evaluation of individuals being considered for disease-modifying therapies.
Blood-Based Tau Tests: Plasma p-tau tests, particularly plasma p-tau217 and plasma p-tau181, have emerged as highly promising blood-based biomarkers for Alzheimer’s disease. These tests serve as proxies not only for tau pathology but also, interestingly, for amyloid burden, because tau phosphorylation in blood appears to be partly driven by amyloid in the brain. This makes plasma p-tau tests particularly useful as a surrogate measure for overall Alzheimer’s pathology burden.
The “N” in ATN refers to evidence of neurodegeneration or neuronal injury, reflecting the downstream consequence of amyloid and tau pathology: the loss of neurons. Biomarkers in this category include:
Structural MRI: Magnetic resonance imaging of the brain can reveal cerebral atrophy, particularly in the hippocampus and entorhinal cortex, which are disproportionately affected in Alzheimer’s disease. However, it is important to acknowledge that structural MRI findings are relatively nonspecific. Brain atrophy is a normal feature of aging, and distinguishing pathological atrophy from age-related changes can be challenging, particularly in older adults. Microvascular changes, white matter hyperintensities, and other structural findings on MRI contribute additional complexity to the interpretation of these scans.
FDG-PET: Fluorodeoxyglucose (FDG) PET imaging measures cerebral glucose metabolism, a surrogate for neuronal activity and health. In Alzheimer’s disease, characteristic patterns of hypometabolism are seen in the posterior cortical regions, including the parietal and temporal lobes. FDG-PET is a sensitive marker of neurodegeneration and correlates well with cognitive performance.
Blood-Based Neurodegeneration Markers: Emerging blood biomarkers for neurodegeneration include neurofilament light chain (NFL) and glial fibrillary acidic protein (GFAP). NFL is a structural component of neurons that is released into the bloodstream when neurons are damaged or dying, making it a marker of active neurodegeneration. Astrocytes release GFAP in response to brain injury or neuroinflammation. While these tests are not yet widely available in standard clinical practice, they represent a rapidly evolving frontier with significant clinical utility in the near future.
When the ATN framework was first published, the initial approach was essentially binary: a patient either had positive or negative amyloid, tau, or neurodegeneration. This was a significant conceptual advance over purely symptom-based diagnosis, but it was still a relatively coarse-grained view of a complex biological reality.
In more recent iterations of the ATN framework and in evolving clinical practice, there is a movement toward quantitative assessment of biomarker burden. Rather than simply asking “does this patient have amyloid?”, we are increasingly asking “how much amyloid does this patient have, and how does that compare to established thresholds and norms?” This quantitative approach provides more nuanced information that can guide treatment decisions and improve prognosis.
This evolution is particularly relevant in the context of the newly approved disease-modifying therapies for Alzheimer’s disease, which have shown the greatest efficacy in patients with specific levels of amyloid burden, and which carry risks (such as amyloid-related imaging abnormalities, or ARIA) that must be carefully weighed against potential benefits. Having quantitative rather than binary biomarker data allows for more individualized risk-benefit analysis.
New technologies and a deeper understanding of the disease process have revolutionized the landscape of Alzheimer’s diagnosis. Recognizing this, a group of experts, supported by the Alzheimer’s Association, developed and published new clinical practice guidelines in 2025 in the journal Alzheimer’s & Dementia. These guidelines, known as DetectAD, provide a structured, evidence-based framework for evaluating cognitive decline.
The guidelines are thoughtfully divided into two tracks: one for primary care clinicians, who are on the front lines of this work, and another for dementia subspecialists. This acknowledges that the bulk of initial evaluations happens in the primary care setting.
The DetectAD framework is built around seven core elements, with the first and last emphasizing the paramount importance of communication.
The DetectAD guidelines include a practical decision tree specifically for primary care. It guides the clinician through a logical sequence of steps. If a patient or the clinician has a concern, the evaluation is initiated. The tree then lays out the components of the evaluation and guidance on when to feel confident in the diagnosis and when to consider consulting a dementia subspecialist.
One of the most valuable parts of this framework is the tiered approach to testing.
It’s crucial to understand that this entire process will likely not happen in a single visit. When a concern for cognitive impairment arises, I often schedule a dedicated, longer follow-up appointment. This allows us to give this complex issue the time and attention it deserves. Studies have shown that patients who voice subjective cognitive concerns to their primary care providers and receive no further evaluation often feel frustrated and dismissed. A dedicated visit honors their concern and sets the stage for a thorough, unhurried investigation.
Understanding the clinical staging of cognitive impairment is essential for several reasons: it determines which diagnostic workup is appropriate, informs which treatments are indicated, shapes how we counsel patients and families, and defines the prognosis. In our practice, we use a structured clinical staging framework that encompasses the full spectrum from normal cognition to advanced dementia.
Normal Cognition: An individual with normal cognition may still harbor significant Alzheimer’s pathology in their brain, as we have discussed with respect to the long preclinical window. However, in the absence of measurable cognitive impairment, the current clinical recommendation is not to pursue biomarker testing routinely. This recommendation reflects both the limitations of our current ability to predict clinical outcomes from preclinical biomarker findings and the potential psychological and social harms of labeling asymptomatic individuals with a diagnosis of preclinical Alzheimer’s disease.
Mild Cognitive Impairment (MCI): MCI represents a critical transitional stage in the Alzheimer’s disease continuum. Individuals with MCI have objectively measurable cognitive changes that are greater than expected for their age and education level, as detected through formal cognitive testing. However, and this is the key distinguishing feature, these individuals remain able to perform their daily activities independently. They may be slower, they may need reminders or strategies, but they are not dependent on others for their basic and instrumental activities of daily living.
MCI due to Alzheimer’s disease (sometimes called amnestic MCI when memory is the primary domain affected) carries a substantially elevated risk of progressing to dementia, with conversion rates estimated at approximately 10 to 15 percent per year in clinic-based samples. Not all individuals with MCI will progress to dementia; some remain stable, and some even show improvement over time, particularly if reversible contributing factors are identified and addressed.
Critically, from a treatment perspective, individuals with MCI due to Alzheimer’s disease represent the most promising target population for the disease-modifying therapies now entering clinical practice. This is because they still have sufficient surviving neurons and cognitive reserve for meaningful benefit from therapies that slow the underlying pathological process.
Dementia: Dementia is diagnosed when an individual has both objectively measured cognitive impairment across one or more domains and functional dependence in their daily activities. The functional criterion is what distinguishes dementia from MCI. The cognitive domains that can be impaired include:
The dementia syndrome is further staged from mild to moderate to severe based on the degree of functional dependence and cognitive impairment, with each stage carrying different treatment priorities and care needs. If a diagnosis of dementia is made, it should be staged as mild, moderate, or severe. This staging is crucial for care planning, prognosis, and ICD-10 coding.
One of the most clinically important, and I would argue underappreciated, findings in dementia research in recent years is the recognition that mixed neuropathology is the rule, not the exception, in older adults with dementia. This insight was powerfully demonstrated in a landmark study published in The Lancet in 2023, which pooled data from six large community-based autopsy cohorts. The results of this study fundamentally challenge the notion that most people with dementia have a single, “pure” neuropathological substrate.
I want to walk through the key findings of this study carefully, because they have profound implications for how we think about diagnosis and treatment in our clinical practice.
When the investigators looked at the distribution of neuropathologies across their large combined cohort, they found that:
Most strikingly, the investigators found that the largest group in the cohort was not any of the single-pathology groups, but rather the group with three or more co-occurring neuropathologies. This finding powerfully illustrates that in real-world clinical populations, particularly in older adults, the brain does not politely confine itself to a single disease process.
The recognition of mixed neuropathology has several important implications for clinical practice that I integrate into my approach at Injury Medical Clinic PA:
Diagnostic humility is essential: Even with the best available biomarker tools, we may not be able to fully characterize all of the neuropathological contributors to a given patient’s cognitive impairment. Current biomarker tests can reliably detect amyloid and tau, and tests for alpha-synuclein and TDP-43 are in development and are expected to reach clinical practice in the coming years. But until we have validated biomarkers for all of the major neuropathologies, our diagnostic picture will remain incomplete for many patients.
Treatment must be guided by symptom expression: When a patient has multiple co-occurring neuropathologies, it is not always possible, or even necessary, to target each one pharmacologically. Instead, treatment decisions should be guided by which symptoms are most prominent, most distressing, and most amenable to intervention. For example, a patient who has both Alzheimer’s and Lewy body pathology may present clinically more like a Lewy body dementia patient, with prominent visual hallucinations and marked sensitivity to antipsychotic medications. In that case, the treatment approach must prioritize the Lewy body clinical features, even if the biomarkers also confirm Alzheimer’s pathology.
Single-agent approaches are rarely sufficient: The complexity of mixed neuropathology supports the rationale for multimodal, comprehensive treatment approaches. No single medication, no single intervention, and no single discipline of care can adequately address the full spectrum of what is happening in a brain affected by multiple co-occurring pathologies. This is one of the core reasons why the integrative model of care we practice at Mission Plaza Injury Medical Clinic in El Paso, incorporating medical oversight, chiropractic care, functional medicine, and rehabilitation, represents a clinically meaningful approach to supporting patients with complex neurological conditions.
The emerging significance of LATE-NC: LATE-NC is worth highlighting because it is a relatively recently described entity now understood to be a major contributor to cognitive impairment in older adults, particularly those over 80. LATE-NC can produce an amnestic syndrome that closely resembles Alzheimer’s disease clinically, but it does not respond to anti-amyloid therapies because it is driven by TDP-43 pathology, not amyloid. As blood-based biomarkers for TDP-43 become available, the ability to distinguish LATE-NC from Alzheimer’s disease will become increasingly important, both for prognosis and for guiding treatment decisions.
The symptomatic pharmacological treatments currently approved for Alzheimer’s disease, as opposed to the disease-modifying therapies, work by targeting the neurotransmitter systems that are disrupted by the underlying neuropathology. To understand why these medications work, why they have the limitations they do, and why additional treatments targeting neuropsychiatric symptoms are often necessary, it is essential to understand the specific neurotransmitter disruptions that occur in Alzheimer’s disease.
The most extensively studied and clinically relevant neurotransmitter disruption in Alzheimer’s disease involves the cholinergic system. Acetylcholine is a neurotransmitter that plays a critically important role in memory, attention, and learning. The major cholinergic projection system that supplies acetylcholine to the cerebral cortex and hippocampus originates from a group of neurons in the basal forebrain, most notably the nucleus basalis of Meynert.
In Alzheimer’s disease, the neurons of the nucleus basalis of Meynert are among the earliest and most severely affected. The destruction of these cholinergic projection neurons results in a profound deficit of acetylcholine in the cerebral cortex and hippocampus, directly impairing memory encoding, attention, and learning that depend on cholinergic neurotransmission.
This observation, first clearly articulated in the late 1970s and early 1980s, gave rise to the cholinergic hypothesis of Alzheimer’s disease and directly motivated the development of the cholinesterase inhibitors (ChEIs), which remain the cornerstone of symptomatic pharmacotherapy for Alzheimer’s disease to this day.
Cholinesterase inhibitors work by inhibiting the enzyme acetylcholinesterase, which is responsible for the breakdown of acetylcholine in the synaptic cleft. By inhibiting this enzyme, ChEIs allow acetylcholine to remain in the synapse longer and stimulate postsynaptic receptors more effectively, partially compensating for the reduction in acetylcholine production resulting from the loss of cholinergic neurons. The three ChEIs currently approved by the FDA for Alzheimer’s disease are donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne). These medications have demonstrated modest but clinically meaningful benefits in cognitive and functional outcomes in patients with mild to moderate and, in the case of donepezil, severe Alzheimer’s disease.
It is important to frame expectations for ChEI therapy with patients and families appropriately. These medications do not stop or reverse the progression of Alzheimer’s disease. They provide symptomatic benefit by enhancing the function of the residual cholinergic neurons that remain, but they cannot prevent the ongoing loss of those neurons. As the disease progresses and more cholinergic neurons are lost, the symptomatic benefit of ChEIs naturally diminishes. Nevertheless, the evidence supports a meaningful functional benefit in terms of daily living activities, and some data suggest benefits for neuropsychiatric symptoms such as apathy and possibly visual hallucinations, which is particularly relevant in patients with Lewy body pathology.
A second major neurotransmitter system disrupted in Alzheimer’s disease is the glutamatergic system. Glutamate is the principal excitatory neurotransmitter in the brain and plays a central role in synaptic plasticity, including long-term potentiation (LTP), which is fundamental to memory formation and learning.
In the Alzheimer’s brain, the normal regulation of glutamate neurotransmission is disturbed. In the context of amyloid and tau pathology, glutamate receptors, particularly N-methyl-D-aspartate (NMDA) receptors, become tonically overactivated by elevated extracellular glutamate levels. This chronic, low-level over-activation of NMDA receptors produces a state of excitotoxicity, in which the excessive influx of calcium ions into neurons triggers mitochondrial dysfunction, oxidative stress, and ultimately cell death. Furthermore, tonic overactivation of NMDA receptors disrupts the normal synaptic signaling required for LTP, effectively “drowning out” the physiological signals that encode new memories.
Memantine (Namenda) is the second major class of FDA-approved symptomatic treatment for Alzheimer’s disease, approved specifically for moderate to severe Alzheimer’s disease. Memantine is an uncompetitive NMDA receptor antagonist that blocks NMDA receptors in a use-dependent manner. This means that memantine preferentially blocks NMDA receptors during the abnormal, tonic low-level activation that occurs in the Alzheimer’s brain, while allowing the strong, phasic activation of NMDA receptors during normal synaptic signaling for memory encoding to proceed. In this way, memantine attempts to restore a more normal signal-to-noise ratio in glutamatergic neurotransmission, reducing excitotoxic neuronal damage while preserving the capacity for physiological learning and memory.
Memantine is often used in combination with cholinesterase inhibitors in patients with moderate to severe Alzheimer’s disease, as the two medications work on different neurotransmitter systems and their effects are additive. The combination of donepezil and memantine has been shown to provide greater benefit than either agent alone in patients with moderate-to-severe disease.
While the cholinergic and glutamatergic systems are the primary pharmacological targets in Alzheimer’s disease, other neurotransmitter systems are also disrupted and contribute importantly to the neuropsychiatric symptom burden of dementia.
Serotonin: The serotonergic system, which plays a major role in mood regulation, anxiety, sleep, and appetite, is significantly disrupted in Alzheimer’s disease. The raphe nuclei in the brainstem, which are the primary source of serotonergic projections to the forebrain, lose neurons in the Alzheimer’s brain. The resulting serotonin deficiency contributes to the high prevalence of depression, anxiety, sleep disturbances, and agitation seen in patients with Alzheimer’s disease. This provides the pharmacological rationale for the use of selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) in managing neuropsychiatric symptoms of dementia.
Dopamine: The dopaminergic system is another important contributor to the neuropsychiatric symptom profile of Alzheimer’s disease. Dopamine pathways originating from the ventral tegmental area and substantia nigra project widely to the frontal cortex and limbic system, where they regulate motivation, reward processing, executive function, and emotional modulation. Disruption of these pathways in Alzheimer’s disease contributes to apathy, which is arguably the single most common and functionally disabling neuropsychiatric symptom in dementia, as well as to other symptoms including psychosis and agitation.
Norepinephrine: The locus coeruleus in the brainstem is the primary source of norepinephrine projections to the cerebral cortex and is, in fact, one of the very first brain regions to show tau pathology in Alzheimer’s disease, even before the hippocampus and entorhinal cortex. The loss of norepinephrine-producing neurons in the locus coeruleus contributes to attention deficits, sleep disturbances, anxiety, and depression in Alzheimer’s disease, and emerging research suggests that norepinephrine has important neuroprotective and anti-inflammatory functions in the brain, meaning that the early loss of locus coeruleus neurons may accelerate the progression of the disease itself.
A structured approach to pharmacological management in dementia requires distinguishing between two broad categories of treatment targets:
Both categories require careful, evidence-based, and individualized pharmacological management and benefit from integration with non-pharmacological interventions, including the structured, multidisciplinary approach we provide at Injury Medical Clinic PA.
The prescribing approach for cognitive symptoms in Alzheimer’s disease follows a relatively well-established evidence base, though clinical judgment and individualization remain essential.
Cholinesterase Inhibitors: All three FDA-approved ChEIs (donepezil, rivastigmine, and galantamine) have demonstrated comparable efficacy in head-to-head studies, with no single agent consistently showing superior cognitive benefits over the others. The choice between agents is therefore guided primarily by considerations of tolerability, formulation, and practical administration factors:
The common side effects of all ChEIs reflect the peripheral consequences of increased cholinergic activity: nausea, vomiting, diarrhea, anorexia, weight loss, and vivid dreams. These are typically most pronounced during dose titration and often improve as the patient adjusts to the medication. More serious side effects include bradycardia and syncope (due to cholinergic slowing of the heart rate), which require particular caution in patients with known cardiac conduction abnormalities.
Memantine: The prescribing approach for memantine in moderate to severe Alzheimer’s disease involves starting at a low dose (5 mg once daily) and titrating gradually to the target dose of 10 mg twice daily over four weeks. Memantine is generally well tolerated, with the most commonly reported side effects being dizziness, headache, constipation, and confusion (paradoxically, since it is used to treat cognitive impairment). The combination of memantine with a ChEI is well-supported by evidence and is generally the standard of care for patients with moderate to severe Alzheimer’s disease.
Neuropsychiatric symptoms (NPS) are present in the vast majority of individuals with dementia at some point in the course of their illness. Epidemiological studies suggest that up to 90 percent of individuals with Alzheimer’s disease will experience at least one neuropsychiatric symptom during the course of their illness, and these, in my clinic and across the literature, neuropsychiatric symptoms—agitation, disinhibition, anxiety and depression, psychosis, sleep disturbance, apathy, mood lability—predict caregiver burnout, emergency department use, and institutionalization. They are the symptoms caregivers fear most and the ones they remember when they describe crises.
The spectrum of NPS in dementia includes:
A structured approach to managing NPS begins with non-pharmacological interventions as the first-line strategy, with pharmacological treatment reserved for symptoms that are severe, persistent, causing significant distress or safety concerns, and have not responded to non-pharmacological approaches. This hierarchy is important for several reasons: many pharmacological agents used to treat NPS in dementia carry significant risks in older adults, and the evidence base for many of these agents in the dementia context is limited.
Non-pharmacological approaches for NPS include structured activity programs, music therapy, reminiscence therapy, modification of the care environment, caregiver education and skills training, light therapy, and regular physical activity. These approaches can be highly effective for mild-to-moderate NPS and should always be incorporated alongside pharmacological management when the latter is pursued.
When pharmacological treatment is indicated for NPS, the specific medication selected should be matched to the specific symptom being targeted:
For depression and anxiety: SSRIs such as sertraline and citalopram are generally considered first-line agents for depression and anxiety in dementia, based on their relatively favorable tolerability profile in older adults and the evidence available from randomized controlled trials in this population. Escitalopram may be preferred for some patients due to its somewhat cleaner pharmacological profile. However, clinicians should be aware of the risk of QTc prolongation with citalopram and escitalopram, which necessitates periodic ECG monitoring in older adults. Venlafaxine and duloxetine (SNRIs) are reasonable alternatives, particularly when anxiety is a prominent feature. Mirtazapine may be beneficial when sedation, appetite stimulation, or improvement in sleep is also desired.
For agitation: The management of agitation in dementia is one of the most challenging and clinically important areas of dementia pharmacotherapy. The evidence base for most pharmacological agents used for agitation in dementia is limited, and many agents carry significant risks. The first new medication specifically FDA-approved for treating agitation associated with Alzheimer’s disease is brexpiprazole (Rexulti), which received this indication in 2023. Brexpiprazole is an atypical antipsychotic with a favorable receptor-binding profile (partial agonism at D2, D3, and serotonin 1A receptors, antagonism at serotonin 2A and 2B receptors) that distinguishes it somewhat from other atypical antipsychotics. It has demonstrated efficacy in reducing agitation in clinical trials and is generally better tolerated than many alternatives.
Other agents used off-label for agitation in dementia include quetiapine, risperidone, olanzapine, and other atypical antipsychotics. However, it is critical to note that all antipsychotic medications carry an FDA black box warning for use in older adults with dementia-related psychosis, specifically the warning that these agents are associated with an increased risk of death (primarily from cardiovascular events and pneumonia). This warning requires that atypical antipsychotics be prescribed judiciously in this population, with explicit discussion of risks and benefits with patients and families, and with careful monitoring.
Citalopram has also shown some evidence of benefit for agitation in Alzheimer’s disease, with a somewhat more favorable risk profile than antipsychotics. However, concerns about QTc prolongation at higher doses limit the doses that can be safely used.
Dextromethorphan/quinidine (Nuedexta), FDA-approved for pseudobulbar affect, is increasingly being studied and used off-label for agitation in dementia, with some promising signals in clinical trial data.
For psychosis: Psychosis in dementia, including delusions and hallucinations, may warrant pharmacological treatment with atypical antipsychotics when the symptoms are causing significant distress or safety concerns, again bearing in mind the black box warning. In patients with Lewy body dementia, special caution is required because these patients can have catastrophic sensitivity reactions to antipsychotic medications; quetiapine or clozapine at very low doses are sometimes used in this population, with extreme caution.
For sleep disturbances: Sleep disturbances are extremely common in Alzheimer’s disease and can significantly worsen caregiver burden. Melatonin and low-dose melatonin receptor agonists (ramelteon) are often used as first-line agents given their favorable safety profiles. Suvorexant (Belsomra), an orexin receptor antagonist, received an FDA-approved indication for insomnia in Alzheimer’s disease in 2022 and represents an evidence-based option. Mirtazapine at low doses (7.5 to 15 mg) is also commonly used for its sedating properties and may simultaneously benefit mood and appetite. Benzodiazepines and non-benzodiazepine sedative-hypnotics (Z-drugs) should generally be avoided in older adults with dementia due to the significant risks of falls, confusion, and paradoxical agitation.
For apathy: Apathy is the most common neuropsychiatric symptom in Alzheimer’s disease and is one of the most difficult to treat. There is no FDA-approved medication specifically for apathy in Alzheimer’s disease. Methylphenidate has the most evidence among pharmacological agents for apathy in this population, with several trials showing modest but meaningful reductions in apathy symptoms, and it is generally well tolerated in the short term. Brexpiprazole has also shown some signals of benefit for apathy in Alzheimer’s disease, though its primary approved indication is for agitation. Structured physical activity and social engagement remain important components of the management of apathy.
For decades, the pharmacological management of Alzheimer’s disease was confined entirely to symptomatic treatments: medications that improved cognitive and functional symptoms without altering the underlying trajectory of the disease. The development of truly disease-modifying treatments, agents that actually slow or arrest the pathological process of Alzheimer’s disease, was an elusive goal that consumed enormous research resources and suffered a long string of high-profile clinical trial failures. These failures are now largely understood in retrospect to have resulted from treating patients who were too far advanced in their disease, when too much neuronal damage had already occurred to allow a meaningful response.
The shift toward biomarker-based diagnosis and the identification of patients in the early stages of the Alzheimer’s disease continuum, specifically those with MCI due to Alzheimer’s disease or early Alzheimer’s dementia, with confirmed amyloid pathology on biomarker testing, has been the critical enabling factor in the successful development of the first disease-modifying therapies.
The disease-modifying therapies that have achieved FDA approval to date all belong to the class of anti-amyloid monoclonal antibodies. These are biologics, large protein molecules derived from immune cell technology, that bind specifically to forms of beta-amyloid in the brain and promote their clearance. The first agents in this class to achieve FDA approval for Alzheimer’s disease are lecanemab (Leqembi) and donanemab (Kisunla), with aducanumab (Aduhelm) having received accelerated approval in 2021 but subsequently being voluntarily withdrawn from the market by its manufacturer.
Lecanemab is a monoclonal antibody that preferentially binds to soluble amyloid protofibrils, which are considered among the most neurotoxic forms of amyloid. In the landmark Phase 3 clinical trial (CLARITY AD), lecanemab was shown to reduce brain amyloid burden by approximately 60 percent over 18 months and to slow the rate of clinical decline on a composite measure of cognitive and functional outcomes (Clinical Dementia Rating Sum of Boxes, CDR-SB) by approximately 27 percent compared to placebo.
Lecanemab received traditional FDA approval in July 2023, having met the FDA’s standards for both surrogate biomarker efficacy (amyloid reduction) and clinical meaningful benefit (slowing of clinical decline). It is administered as an intravenous infusion every two weeks. It requires confirmatory biomarker evidence of amyloid pathology (via CSF, PET, or blood-based tests, as part of the clinical protocol) before initiation.
A critical safety consideration with lecanemab, as with all anti-amyloid monoclonal antibodies, is the risk of ARIA (Amyloid-Related Imaging Abnormalities). ARIA refers to a spectrum of MRI-detected abnormalities associated with the rapid clearance of amyloid from the brain, including:
In the CLARITY AD trial, ARIA was detected on MRI in approximately 21 percent of lecanemab-treated patients, compared to approximately 9 percent in the placebo group. The majority of ARIA events were asymptomatic or produced only mild, transient symptoms, but serious and, in some cases, severe ARIA events occurred in a minority of patients. ARIA risk is significantly elevated in patients who carry the APOE e4 allele, particularly in homozygous APOE e4/e4 carriers.
This means that APOE genotyping is an important consideration in the clinical workup before initiating lecanemab, and that APOE e4/e4 homozygous individuals require particularly careful and detailed risk-benefit counseling before starting treatment.
Donanemab is another anti-amyloid monoclonal antibody that targets a specific form of amyloid known as pyroglutamate amyloid, which is found specifically within amyloid plaques (as opposed to soluble amyloid). This targeting strategy means that donanemab is particularly effective at removing plaque-deposited amyloid, and the pharmacokinetic consequence is that once amyloid plaques have been cleared to below the threshold of positivity on amyloid PET, the treatment can be discontinued, as donanemab has essentially “run out of target.” This has the clinically significant implication that some patients may be able to complete treatment and discontinue the infusions.
In the landmark Phase 3 TRAILBLAZER-ALZ 2 trial, donanemab demonstrated a 35 percent slowing of clinical decline on the integrated Alzheimer’s Disease Rating Scale (iADRS) in the overall study population and even greater efficacy in the subgroup of patients with lower baseline tau burden (47 percent slowing on iADRS). These results support the important clinical message that the earlier in the disease course treatment is initiated, the greater the potential benefit, since patients with lower tau burden are earlier in the disease trajectory.
Donanemab is administered as an intravenous infusion every four weeks, which is less frequent than lecanemab’s every-two-week schedule and may be more convenient for patients and caregivers. Like lecanemab, donanemab carries a risk of ARIA, with ARIA-E rates of approximately 24 percent and ARIA-H rates of approximately 31 percent in the TRAILBLAZER-ALZ 2 trial. As with lecanemab, most ARIA events were asymptomatic or mildly symptomatic.
Given the requirements of pivotal clinical trials and FDA labeling for these agents, specific criteria define which patients are the most appropriate candidates for DMT therapy. These include:
Given the clinical complexity of patient selection for DMTs, the need for biomarker confirmation, APOE genotyping, baseline neuroimaging, and ongoing safety monitoring, the initiation and management of DMT therapy for Alzheimer’s disease is most appropriately conducted in a setting with access to specialist-level expertise in cognitive neurology or geriatric psychiatry, along with access to the requisite neuroimaging capabilities and laboratory testing.
In primary care settings, the critical role of the primary care clinician and the broader care team is to:
This is precisely the model of care we strive to implement at Injury Medical Clinic PA in El Paso, Texas, where my own clinical practice integrates primary care, specialty-level cognitive assessment, and functional medicine, all under the collaborative oversight of Dr. Maria Guadalupe Cardenas, MD, our Medical Director.
Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, located in El Paso, Texas, represents a model of integrative, multidisciplinary healthcare that I believe is ideally suited to the complex needs of patients living with conditions such as Alzheimer’s disease, related dementias, and the many co-occurring conditions that frequently accompany them. Our clinic brings together expertise from multiple disciplines, including chiropractic care, internal medicine, functional medicine, personal injury rehabilitation, and nutritional and lifestyle medicine, under one clinical umbrella, with the shared goal of providing each patient with the most comprehensive, evidence-based, and individualized care possible.
This multidisciplinary model is increasingly recognized in the scientific literature as the most effective approach for managing complex, chronic, and multifactorial conditions. Alzheimer’s disease and related dementias are a paradigmatic example of why such an approach is necessary: these conditions affect not only the brain but the whole person, including their cardiovascular health, metabolic function, musculoskeletal system, nutritional status, sleep, stress physiology, and social and emotional well-being. No single discipline of care can adequately address all of these dimensions simultaneously.
Central to our clinic’s integrative model is the leadership and expertise of Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933), who serves as our Medical Director and Collaborative Physician. Dr. Cardenas is Board Certified in Internal Medicine and brings over 40 years of clinical experience as a practicing internist to our team. Her depth of knowledge in internal medicine, her extensive experience managing complex multi-system conditions in older adults, and her commitment to patient-centered, evidence-based care make her an invaluable foundation of our multidisciplinary team.
In the context of dementia care specifically, Dr. Cardenas’s expertise is crucial for several reasons:
The collaborative relationship between Dr. Cardenas and me, Dr. Alex Jimenez, DC, APRN, FNP-BC, reflects a model of care that is increasingly common and recognized in integrative and functional medicine settings: a physician with broad medical expertise providing direction and oversight alongside a clinician with specialized training in chiropractic, advanced practice nursing, and functional medicine. This combination allows our practice to address the full spectrum of a patient’s needs, from the purely medical to the functional, rehabilitative, and preventive.
My own clinical approach at Injury Medical Clinic PA reflects the unique synthesis of training and expertise that I bring to patient care: board certification in chiropractic care, advanced practice registered nursing as a Family Nurse Practitioner (FNP-BC), and specialized training in functional medicine (CFMP, IFMCP), sports nutrition (ATN), clinical sports science (CCST), and advanced diagnostics. This combination allows me to evaluate and treat patients through multiple clinical lenses simultaneously, identifying and addressing not only the primary presenting condition but also the underlying metabolic, nutritional, inflammatory, and structural factors that contribute to their overall health and cognitive function.
In my clinical observations, which I document and share through platforms such as PushAsRx.com and my LinkedIn profile, I have consistently found that patients with neurological conditions, including those on the Alzheimer’s disease spectrum, often present with a constellation of contributing factors that extend well beyond the neurological diagnosis itself. These include:
Addressing these contributing factors through the combination of chiropractic care, functional medicine interventions, nutritional optimization, and rehabilitative exercise is a core component of the comprehensive care I provide for patients with cognitive concerns at our clinic.
The connection between chiropractic care and brain and cognitive health may not be immediately obvious to those unfamiliar with the broader functional and integrative medicine literature. However, there is a growing body of evidence and a coherent theoretical framework linking the two, and I believe it is important to articulate this connection clearly, as it forms a significant part of the rationale for the integrative approach we take at our clinic.
Chiropractic care is grounded in the principle that the structural integrity of the musculoskeletal system, and particularly the spinal column and nervous system, plays a central role in overall health and physiological function. The spine houses and protects the spinal cord, a critical component of the central nervous system, and the vertebral column and associated structures have important relationships with the autonomic nervous system, cerebrospinal fluid dynamics, and the regulation of neuroinflammation.
Cervical Spine Health and Cerebral Blood Flow: The cervical spine (neck region) has a particularly important relationship with brain health due to its anatomical proximity to the vertebral arteries, which provide approximately 20 percent of the brain’s blood supply through the vertebrobasilar circulation. Degenerative changes in the cervical spine, including osteoarthritis, disc herniation, and vertebral misalignment (subluxation), can compromise vertebral artery flow and reduce cerebral perfusion in posterior brain regions. While the relationship between cervical spine pathology and cognitive function remains an area of active investigation, the physiological plausibility is established, and clinical evidence suggests that cervical spine dysfunction is not infrequent in older adults with cognitive decline.
Chiropractic manipulation and mobilization of the cervical spine aim to restore normal joint mechanics, reduce pain and muscle tension, and potentially improve vertebral artery flow and autonomic nervous system function. In my clinical practice, I routinely assess the cervical spine in patients with cognitive concerns and, when indicated, incorporate appropriate chiropractic interventions alongside the medical management provided by Dr. Cardenas.
Cerebrospinal Fluid Dynamics and Spinal Health: An emerging and fascinating area of research involves the relationship between spinal mechanics and cerebrospinal fluid (CSF) flow dynamics. CSF is the fluid that bathes the brain and spinal cord, providing buoyancy, nutrient delivery, and critically, waste clearance from the brain. The glymphatic system, a recently discovered brain-wide waste-clearance system that operates primarily during sleep, clears toxic proteins, including beta-amyloid and tau, from the brain parenchyma into the CSF for eventual elimination.
Research has suggested that CSF flow dynamics are influenced by spinal mechanics, particularly the normal thoracic and lumbar pump mechanisms that occur during breathing and movement. Dysfunction in these mechanisms, whether due to spinal restriction, poor posture, or reduced physical activity, may impair the efficiency of the glymphatic waste-clearance system, potentially contributing to the accumulation of amyloid and tau in the brain. Maintaining spinal mobility and function through chiropractic care and rehabilitative exercise may therefore have indirect benefits for glymphatic function and brain waste clearance. However, this connection requires further direct investigation in clinical studies.
Autonomic Nervous System Regulation: The autonomic nervous system (ANS) plays a crucial role in neuroinflammation, immune function, cardiovascular regulation, and the stress response, all of which are relevant to the pathophysiology of Alzheimer’s disease. The ANS is regulated in part by spinal cord and brainstem mechanisms, and research suggests that spinal manipulation can modulate autonomic function, including heart rate variability (HRV), a measure of autonomic balance. Improving ANS regulation through chiropractic care may help reduce chronic neuroinflammation and support the brain’s own neuroprotective mechanisms.
Pain Management and Cognitive Function: Chronic pain is extremely common in older adults and is an important and often underappreciated contributor to cognitive impairment. Chronic pain activates the stress response (HPA axis), drives systemic inflammation, disrupts sleep, impairs attention and executive function, and competes with cognitive resources. Research has demonstrated that chronic pain and dementia frequently co-occur and that the presence of chronic pain can worsen cognitive outcomes in individuals with Alzheimer’s disease. Effective management of chronic musculoskeletal pain through chiropractic care, manual therapy, and rehabilitation can therefore have meaningful downstream benefits for cognitive function and quality of life in patients with dementia.
Physical Activity and Neuroplasticity: One of the most robust findings in the neuroscience of aging is that regular physical activity is strongly associated with reduced risk of dementia and may slow cognitive decline in individuals with early Alzheimer’s disease. Physical activity promotes the production of brain-derived neurotrophic factor (BDNF), a key molecular mediator of neuroplasticity, synaptic health, and neurogenesis, particularly in the hippocampus. It also improves cardiovascular health, reduces inflammation, improves insulin sensitivity, enhances sleep quality, and reduces depression and anxiety, all of which are beneficial for brain health.
Chiropractic care and rehabilitative exercise programs, as practiced at our clinic, play an important role in enabling older adults with musculoskeletal conditions to engage in regular physical activity. By reducing pain, improving mobility, restoring functional movement patterns, and providing supervised exercise programming, we remove barriers to physical activity that would otherwise prevent our patients from accessing one of the most potent and well-evidenced interventions available for brain health.
Functional medicine is a systems-oriented, personalized approach to medicine that seeks to identify and address the root causes of disease, rather than simply managing symptoms. In the context of Alzheimer’s disease, functional medicine approaches are grounded in the growing recognition that Alzheimer’s disease is not simply a genetic inevitability but rather a complex, multifactorial condition in which modifiable metabolic, inflammatory, nutritional, hormonal, and lifestyle factors play important roles in both disease risk and disease progression.
The seminal work of Dr. Dale Bredesen, particularly his ReCODE (Reversal of Cognitive Decline) protocol, has drawn considerable attention to the potential of comprehensive, functional medicine-based interventions to influence the trajectory of early Alzheimer’s disease. While the ReCODE protocol remains controversial in some quarters due to the nature of the evidence supporting it (primarily case series and small trials rather than large RCTs), it has stimulated important thinking about the many metabolic and lifestyle factors that converge to either protect the brain or leave it vulnerable to Alzheimer’s pathology.
At Injury Medical Clinic PA, my functional medicine approach to patients with cognitive concerns focuses on the following key domains:
Metabolic and Vascular Health: There is compelling epidemiological and mechanistic evidence linking insulin resistance, type 2 diabetes, hypertension, dyslipidemia, and obesity to increased Alzheimer’s disease risk. Insulin resistance in the brain, sometimes referred to as “type 3 diabetes” in the lay literature, impairs the brain’s ability to use glucose as fuel, reduces the production of neuroprotective factors, and promotes amyloid accumulation. Optimizing metabolic health through dietary interventions (particularly low-glycemic index, anti-inflammatory dietary patterns), physical activity, and appropriate pharmacological management by Dr. Cardenas is a cornerstone of our approach.
Nutritional Optimization: Several nutritional factors have been associated with brain health and dementia risk:
Inflammation Management: Neuroinflammation is now recognized as a central and self-perpetuating contributor to Alzheimer’s disease pathology. Activated microglia, the brain’s resident immune cells, and astrocytes drive an inflammatory response in the Alzheimer’s brain that contributes to synaptic dysfunction and neuronal death. Systemic inflammation, driven by factors such as periodontal disease, obesity, gut dysbiosis, and chronic stress, can cross-communicate with the brain and amplify neuroinflammation. Our functional medicine approach identifies and addresses modifiable drivers of systemic inflammation, including dietary modification, targeted supplementation, stress management, sleep optimization, and treatment of chronic infections.
Sleep Optimization: Sleep is not merely a period of rest for the brain. As noted earlier, the glymphatic system operates primarily during sleep, clearing amyloid and tau from the brain. Sleep deprivation and sleep disorders, particularly obstructive sleep apnea, are associated with increased amyloid accumulation and elevated dementia risk. Screening for and treating sleep disorders, optimizing sleep hygiene, and addressing musculoskeletal factors that may contribute to sleep disruption (such as chronic pain or cervical spine dysfunction) are all important components of our care.
Hormonal Balance: Several hormonal systems have relevance to brain health and Alzheimer’s disease risk, including thyroid hormone (hypothyroidism is a recognized cause of reversible cognitive impairment), sex hormones (the decline of estrogen at menopause has been associated with increased Alzheimer’s risk in women, who represent approximately two-thirds of all Alzheimer’s cases), and cortisol (chronic stress and elevated cortisol promote hippocampal atrophy and impair cognitive function). Assessment and management of hormonal imbalances is part of our comprehensive functional medicine evaluation.
Gut-Brain Axis: Emerging research is rapidly advancing our understanding of the gut-brain axis in the context of Alzheimer’s disease. The gut microbiome appears to play a role in regulating neuroinflammation, amyloid metabolism, and cognitive function through multiple pathways including the vagus nerve, the immune system, and microbial metabolites such as short-chain fatty acids. Gut dysbiosis and increased intestinal permeability (“leaky gut”) may contribute to systemic inflammation and neuroinflammation in Alzheimer’s disease. Our functional medicine approach includes assessment of gut health and microbiome-targeted interventions where indicated.
One of the most important and clinically actionable bodies of evidence in dementia research is the Lancet Commission on Dementia Prevention, Intervention, and Care, which has been updated periodically and now identifies twelve modifiable risk factors that together account for approximately 40 percent of dementia cases worldwide. This means that up to 40 percent of dementia cases could theoretically be prevented or delayed by addressing these modifiable risk factors. The twelve risk factors identified are:
Each of these risk factors has a plausible, often well-characterized biological mechanism that contributes to dementia risk, and each is, to varying degrees, modifiable through clinical intervention, lifestyle change, and public health measures.
At Injury Medical Clinic PA, the comprehensive, multidisciplinary nature of our clinical approach means that we are uniquely positioned to address many of these risk factors simultaneously. For example:
Traumatic brain injury (TBI) warrants special mention given our clinic’s focus on personal injury care. TBI is recognized as a significant modifiable risk factor for Alzheimer’s disease and other dementias, with the relationship between TBI severity, frequency, and dementia risk being well-documented in the epidemiological literature. The mechanisms through which TBI increases dementia risk include:
In my personal injury care practice, the management of TBI and its sequelae is conducted with a thorough understanding of these long-term risks. Comprehensive, evidence-based rehabilitation following TBI, including both chiropractic care for musculoskeletal and neurological components and medical management by Dr. Cardenas, is not only about immediate symptom management, but also about potentially mitigating the long-term neurological consequences of the injury. This is a clinically important dimension of our work that I believe has significant public health implications, particularly given the prevalence of TBI in motor vehicle accidents, sports injuries, and occupational injuries in our patient population in El Paso.
Apolipoprotein E (APOE) is a protein involved in the transport and metabolism of lipids, including cholesterol, in the brain and peripherally. The gene encoding APOE exists in three common allelic variants: e2, e3, and e4. Every individual inherits two copies of the APOE gene, one from each parent, leading to six possible genotype combinations.
The APOE alleles have dramatically different impacts on Alzheimer’s disease risk:
It is critically important to emphasize that APOE e4 is not deterministic: many APOE e4 carriers never develop Alzheimer’s disease, and conversely, many people who develop Alzheimer’s disease do not carry the APOE e4 allele. APOE e4 is a risk modifier, not a genetic sentence.
As discussed earlier in this post, APOE e4 status significantly modifies the risk of ARIA associated with anti-amyloid monoclonal antibodies. This is because APOE e4 is associated with greater cerebral amyloid angiopathy (CAA), a condition in which amyloid deposits in the walls of cerebral blood vessels. When anti-amyloid therapies rapidly clear amyloid from both parenchymal plaques and vessel walls, the sudden mobilization of amyloid can cause vasogenic edema and microhemorrhages (ARIA) in individuals with CAA. The higher the CAA burden, the greater the ARIA risk.
APOE e4/e4 homozygotes have substantially higher rates of ARIA in DMT trials. For example, in the TRAILBLAZER-ALZ 2 trial with donanemab, ARIA rates were approximately 36 percent in APOE e4/e4 individuals compared to approximately 20 percent in non-carriers. Serious ARIA events, including fatal ARIA, were more frequent in APOE e4/e4 individuals. This means that the decision to initiate DMT in APOE e4/e4 homozygous individuals requires particularly careful and detailed risk-benefit counseling and close monitoring.
Communicating APOE genotype results to patients and families requires great care and skill. For some individuals, learning that they carry the APOE e4 allele may cause significant anxiety or depression, particularly if they already have a family member with Alzheimer’s disease. At the same time, this information, when appropriately contextualized, can be empowering: it can motivate individuals to address modifiable risk factors more aggressively and engage in lifestyle modifications that may reduce their risk.
In our practice, the communication of genetic risk information is conducted with careful attention to the patient’s emotional readiness, within a comprehensive genetic counseling framework, and with explicit discussion that APOE e4 is a risk factor, not a definitive diagnosis of future Alzheimer’s disease.
In primary care settings, patients presenting with cognitive concerns can be broadly grouped into two clinical scenarios that require somewhat different evaluation approaches:
Scenario 1: New Cognitive Complaints in the Context of a General Primary Care Visit
This is the more common scenario in most primary care practices: a patient, or more often a family member accompanying the patient, raises concerns about memory, word-finding difficulties, getting lost in familiar places, or changes in behavior. In this scenario, the primary care clinician’s role is to:
Scenario 2: Structured Evaluation for Suspected Alzheimer’s Disease with Biomarker Assessment
In settings where the clinical presentation is more specifically concerning for Alzheimer’s disease and access to biomarker testing is available, the evaluation includes pathological biomarker assessment, as described in the ATN framework. This may include blood-based amyloid and tau tests (as a first-line screening step), followed by CSF or PET confirmation when indicated. This structured biomarker evaluation is particularly important when the patient may be a candidate for disease-modifying therapy.
One of the challenges in primary care cognitive evaluation is the time required to administer and score traditional cognitive assessment tools. Digital cognitive assessment tools, such as Brain Check, are addressing this challenge by automating the administration and scoring of validated cognitive tests, reducing the burden on clinicians, and potentially improving the sensitivity and reproducibility of cognitive screening in busy primary care settings. These tools can administer multiple validated cognitive tests in a relatively short time, generate automated scores and interpretations, and track change over time, all of which facilitate more systematic and efficient cognitive monitoring in primary care.
A significant portion of the patients I see at Injury Medical Clinic PA are referred for evaluation and treatment of injuries sustained in motor vehicle accidents, workplace injuries, slip-and-fall accidents, and sports injuries. Many of these patients have sustained injuries to the head, neck, and spine, which, as discussed in detail earlier in this post, have direct implications for neurological health, brain perfusion, CSF dynamics, and long-term dementia risk.
The intersection of personal injury care and cognitive health is an area that I believe deserves far more clinical attention than it currently receives in standard personal injury management. Many personal injury patients who have sustained mild traumatic brain injury (concussion) or cervical spine injuries are managed primarily from a symptomatic and medicolegal perspective, with relatively little attention paid to the long-term neurological implications of their injuries.
At our clinic, our approach to personal injury care integrates:
This comprehensive approach to personal injury care reflects our belief that the standard of care for personal injury patients should encompass not just acute symptom management, but genuine long-term health optimization and neuroprotection.
While the anti-amyloid monoclonal antibodies represent the first wave of approved disease-modifying therapies for Alzheimer’s disease, the research pipeline is actively developing therapies that target tau pathology as well. Tau is particularly attractive as a therapeutic target because the severity of tau pathology correlates more closely with cognitive decline than amyloid burden does, making tau a more direct driver of the neurodegeneration that produces clinical symptoms.
Anti-tau monoclonal antibodies targeting different forms of tau, including extracellular tau aggregates, have been in clinical trials. Several of these have not yet demonstrated efficacy at the doses and stages tested, but the field is actively learning from these trials and refining the targeting strategies, patient selection criteria, and outcome measures.
Tau aggregation inhibitors represent a small molecule approach to disrupting tau aggregation and tangle formation. These agents aim to prevent tau from misfolding and self-aggregating, rather than clearing already-formed tangles.
Antisense oligonucleotides (ASOs) targeting tau are another promising approach in which small DNA-like molecules are introduced into the CSF to reduce tau production in neurons, potentially preventing tangle formation before it occurs.
TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) is a receptor expressed on microglia, the brain’s resident immune cells, that plays a critical role in regulating the microglial response to amyloid and damaged neurons. Loss-of-function variants in the TREM2 gene are among the genetic risk factors for late-onset Alzheimer’s disease. Therapeutic strategies that activate or enhance TREM2 signaling in microglia may improve the brain’s ability to clear amyloid and tau pathology while modulating the neuroinflammatory response. Anti-TREM2 agonist antibodies and other TREM2-targeting agents are currently in early-phase clinical trials.
As discussed throughout this post, blood-based biomarkers for Alzheimer’s disease are advancing rapidly. The clinical utility of plasma p-tau217, plasma amyloid-beta 42/40 ratio, and other markers is being validated in large-scale studies. The goal is to develop blood-based biomarker tests with sufficient sensitivity, specificity, and accessibility to serve as a first-line screening tool in primary care, enabling earlier identification of individuals with Alzheimer’s pathology who might benefit from lifestyle interventions, risk factor management, or eventually, disease-modifying treatment.
In my clinical practice, I anticipate that the availability of reliable, affordable, and minimally invasive blood-based biomarker tests will transform the early detection of Alzheimer’s disease in the primary care setting over the next few years, much as lipid panels transformed the early detection and management of cardiovascular risk.
Just as cancer treatment has moved from single-agent chemotherapy to complex multi-drug, multi-target combination regimens, it is widely anticipated that the most effective treatments for Alzheimer’s disease will eventually involve combination approaches that simultaneously target multiple pathological processes: amyloid, tau, neuroinflammation, metabolic dysfunction, and others. The recognition, as described in the Lancet 2023 autopsy study discussed earlier in this post, that most individuals with dementia have multiple co-occurring neuropathologies further supports the rationale for combination therapeutic strategies.
The development of effective combination therapies requires, among other things, the availability of sensitive and specific biomarkers that can track the effects of each component of a combination treatment on its specific target, enabling dose optimization and personalized treatment selection. The field is making rapid progress toward this goal, and I expect that the coming decade will see the emergence of increasingly sophisticated precision-medicine-based approaches to Alzheimer’s disease treatment.
The availability of biomarker tests that can detect Alzheimer’s pathology years to decades before symptoms develop raises profound ethical questions that our field is actively grappling with. If a person has a positive amyloid blood test but no cognitive symptoms, should they be told? What are the psychological, social, and economic consequences of being labeled as having “preclinical Alzheimer’s disease”? How do we ensure that this information is communicated in a way that is genuinely useful and not simply anxiety-provoking or stigmatizing?
The current consensus, as noted earlier in this post, is that biomarker testing should be performed only in individuals with symptomatic cognitive changes, and that the results should be communicated in the context of comprehensive, expert clinical support. As the field progresses and treatment options expand, the calculus around pre-symptomatic testing may shift, but for now, a careful approach is warranted.
The diagnosis of Alzheimer’s disease, particularly at an early stage when the individual still has substantial decision-making capacity, represents a unique and precious window for advance care planning. Early-stage patients can meaningfully participate in discussions about their wishes for future medical care, including decisions about the use of life-sustaining treatments, preferences for care setting (home vs. facility), designation of a durable power of attorney for healthcare, and preferences about participation in clinical research.
At Injury Medical Clinic PA, we facilitate these conversations proactively, in collaboration with our patients and their families, ensuring that the patient’s voice and values are documented and honored as the disease progresses and decision-making capacity diminishes.
The disease-modifying therapies now available for Alzheimer’s disease are extraordinarily expensive (lecanemab’s list price is approximately $26,500 per year), require specialized monitoring infrastructure (infusion centers and frequent MRI monitoring), and are most readily accessible at well-resourced academic medical centers in urban areas. This creates significant concerns about health equity: will the patients who could most benefit from these treatments, including underrepresented racial and ethnic minorities, rural populations, and individuals of lower socioeconomic status, actually be able to access them?
As clinicians practicing in El Paso, Texas, a predominantly Hispanic border community with significant socioeconomic diversity and health disparities, these concerns are not abstract for us. Dr. Cardenas and I are deeply committed to advocating for and actively facilitating equitable access to comprehensive dementia evaluation and treatment for all of our patients, regardless of their insurance status, socioeconomic background, or geographic access to academic medical centers.
Alzheimer’s disease is not just a disease of the individual who carries the diagnosis. It profoundly affects the family members and other informal caregivers who provide the vast majority of day-to-day care and support for people living with the disease. An estimated 11 million Americans provide unpaid care for individuals with Alzheimer’s disease or other dementias, and the physical, emotional, and financial burden of caregiving is substantial.
Caregiver burden is associated with elevated rates of depression, anxiety, physical illness, social isolation, and financial strain in family caregivers, and the stress of caregiving can itself have negative health consequences, including increased cardiovascular risk and accelerated aging. Importantly, the well-being of the caregiver is a critical determinant of the quality of care that the person with dementia receives, as well as the ability to maintain the person with dementia in their home community rather than requiring nursing home placement.
At Injury Medical Clinic PA, we explicitly incorporate caregiver support and education into our dementia care model. This includes:
Dr. Cardenas’s expertise in internal medicine is particularly valuable in this context, as many family caregivers are themselves older adults with their own complex medical needs that require attention alongside their caregiving responsibilities.
The landscape of Alzheimer’s disease diagnosis and treatment has changed profoundly in recent years, and it is continuing to evolve rapidly. As I summarize the key clinical takeaways from this comprehensive review, I want to ground them in the practical realities of what they mean for our patients at Injury Medical Clinic PA and for clinicians more broadly.
Diagnosis before treatment is non-negotiable: The accuracy and timing of the Alzheimer’s disease diagnosis have never mattered more than they do today, because the disease-modifying therapies now available are specifically indicated for confirmed amyloid-positive disease at the early stages of the clinical spectrum. Getting the diagnosis right, including biomarker confirmation where appropriate and staging the clinical severity carefully, is the foundation of everything else.
Alzheimer’s disease is biologically complex and begins decades before symptoms: The amyloid cascade begins fifteen to twenty years before clinical symptoms appear, and by the time a patient presents with memory complaints, significant neuronal damage has already occurred. This underscores the importance of early identification, timely biomarker evaluation, and comprehensive risk factor management across the lifespan.
Most patients with dementia have mixed neuropathology: The Lancet 2023 autopsy study powerfully demonstrates that pure Alzheimer’s disease is less common in the real world than we might like, and that most older adults with dementia have multiple co-occurring neuropathological contributors. This reality demands diagnostic humility, symptom-guided treatment prioritization, and multimodal therapeutic approaches.
The ATN framework transforms our diagnostic approach: Moving from purely symptom-based diagnosis to biomarker-anchored diagnosis enables earlier, more accurate, and more personalized disease characterization. Blood-based biomarkers are making this more accessible, though gold-standard confirmation with CSF or PET remains important for high-stakes decisions.
Symptomatic treatment remains essential and should not be neglected in the DMT era: The availability of disease-modifying therapies does not diminish the importance of carefully managing cognitive and neuropsychiatric symptoms with cholinesterase inhibitors, memantine, antidepressants, and other targeted agents. For the majority of patients who are not candidates for DMTs (due to disease stage, comorbidities, or patient preference), symptomatic management remains the primary pharmacological intervention.
Disease-modifying therapies represent a genuine breakthrough but require careful patient selection: Lecanemab and donanemab provide the first genuine pharmacological slowing of Alzheimer’s disease progression, with approximately 27 to 47 percent slowing of clinical decline in appropriately selected patients. The key to appropriate use is early identification, confirmed amyloid positivity, APOE genotyping, and careful ARIA monitoring.
Integrative, multidisciplinary care is not optional; it is necessary: The biological complexity of Alzheimer’s disease, the multiplicity of contributing factors, and the profound impact on the whole person and their family all argue strongly for a comprehensive, integrative model of care. At Injury Medical Clinic PA, our combination of chiropractic care, internal medicine oversight from Dr. Cardenas, functional medicine, rehabilitation, and personal injury care is designed specifically to address this complexity.
Modifiable risk factors account for up to 40 percent of dementia risk: The Lancet Commission’s identification of twelve modifiable risk factors, each with plausible biological mechanisms and evidence-based interventions, provides a powerful framework for preventive care. Many of these risk factors fall squarely within the scope of integrative and primary care practice.
Caregiver support is an essential component of dementia care: The family members and care partners who support people living with Alzheimer’s disease require their own assessment, education, and support, and their well-being is directly linked to the quality of care and quality of life of the patients they support.
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Professional Scope of Practice *
The information herein on "Integrative Therapies and Their Benefits for Cognitive Decline" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.
Blog Information & Scope Discussions
Welcome to El Paso's Premier Fitness, Injury Care Clinic & Wellness Blog, where Dr. Alex Jimenez, DC, FNP-C, a Multi-State board-certified Family Practice Nurse Practitioner (FNP-BC) and Chiropractor (DC), presents insights on how our multidisciplinary team is dedicated to holistic healing and personalized care. Our practice aligns with evidence-based treatment protocols inspired by integrative medicine principles, similar to those found on this site and our family practice-based chiromed.com site, focusing on restoring health naturally for patients of all ages.
Our areas of multidisciplinary practice include Wellness & Nutrition, Chronic Pain, Personal Injury, Auto Accident Care, Work Injuries, Back Injury, Low Back Pain, Neck Pain, Migraine Headaches, Sports Injuries, Severe Sciatica, Scoliosis, Complex Herniated Discs, Fibromyalgia, Chronic Pain, Complex Injuries, Stress Management, Functional Medicine Treatments, and in-scope care protocols.
Our information scope is multidisciplinary, focusing on musculoskeletal and physical medicine, wellness, contributing etiological viscerosomatic disturbances within clinical presentations, associated somato-visceral reflex clinical dynamics, subluxation complexes, sensitive health issues, and functional medicine articles, topics, and discussions.
We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for musculoskeletal injuries or disorders.
Our videos, posts, topics, and insights address clinical matters and issues that are directly or indirectly related to our clinical scope of practice.
Our office has made a reasonable effort to provide supportive citations and has identified relevant research studies that support our posts. We provide copies of supporting research studies upon request to regulatory boards and the public.
We understand that we cover matters that require an additional explanation of how they may assist in a particular care plan or treatment protocol; therefore, to discuss the subject matter above further, please feel free to ask Dr. Alex Jimenez, DC, APRN, FNP-BC, or contact us at 915-850-0900.
We are here to help you and your family.
Blessings
Dr. Alex Jimenez DC, MSACP, APRN, FNP-BC*, CCST, IFMCP, CFMP, ATN
email: coach@elpasofunctionalmedicine.com
Multidisciplinary Licensing & Board Certifications:
Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Texas DC License #: TX5807, Verified: TX5807
New Mexico DC License #: NM-DC2182, Verified: NM-DC2182
Multi-State Advanced Practice Registered Nurse (APRN*) in Texas & Multi-States
Multistate Compact APRN License by Endorsement (42 States)
Texas APRN License #: 1191402, Verified: 1191402 *
Florida APRN License #: 11043890, Verified: APRN11043890 *
Verify Link: Nursys License Verifier
* Prescriptive Authority Authorized
ANCC FNP-BC: Board Certified Nurse Practitioner*
Compact Status: Multi-State License: Authorized to Practice in 40 States*
Graduate with Honors: ICHS: MSN-FNP (Family Nurse Practitioner Program)
Degree Granted. Master's in Family Practice MSN Diploma (Cum Laude)
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
Digital Business Card
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)
(Licensed Medical Doctor)
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426749
MD License #: J2933
Licenses and Board Certifications:
MD: Medical Doctor
DC: Doctor of Chiropractic
APRNP: Advanced Practice Registered Nurse
FNP-BC: Family Practice Specialization (Multi-State Board Certified)
RN: Registered Nurse (Multi-State Compact License)
CFMP: Certified Functional Medicine Provider
MSN-FNP: Master of Science in Family Practice Medicine
MSACP: Master of Science in Advanced Clinical Practice
IFMCP: Institute of Functional Medicine
CCST: Certified Chiropractic Spinal Trauma
ATN: Advanced Translational Neutrogenomics
Memberships & Associations:
TCA: Texas Chiropractic Association: Member ID: 104311
AANP: American Association of Nurse Practitioners: Member ID: 2198960
ANA: American Nurse Association: Member ID: 06458222 (District TX01)
TNA: Texas Nurse Association: Member ID: 06458222
NPI: 1205907805
| Primary Taxonomy | Selected Taxonomy | State | License Number |
|---|---|---|---|
| No | 111N00000X - Chiropractor | NM | DC2182 |
| Yes | 111N00000X - Chiropractor | TX | DC5807 |
| Yes | 363LF0000X - Nurse Practitioner - Family | TX | 1191402 |
| Yes | 363LF0000X - Nurse Practitioner - Family | FL | 11043890 |
| Yes | 363LF0000X - Nurse Practitioner - Family | CO | C-APN.0105610-C-NP |
| Yes | 363LF0000X - Nurse Practitioner - Family | NY | N25929 |
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
Digital Business Card
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)*
(Licensed Medical Doctor)*
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426749
MD License #: J2933
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