Integrative Therapies to Consider for Cognitive Decline

Address cognitive decline with integrative therapies that support cognitive function and improve mental wellness.

Abstract

Welcome to this in-depth exploration of Alzheimer’s disease and related dementias. As Dr. Alex Jimenez, I am honored to guide you through the intricate landscape of modern neurological care. This post will delve into the latest scientific understanding of Alzheimer’s, moving beyond traditional clinical symptom-based diagnoses to a more precise, biomarker-driven approach. We will unravel the complex interplay among proteins such as amyloid and tau, explore the ATN (Amyloid, Tau, Neurodegeneration) framework, and discuss the profound implications of co-occurring neuropathologies that complicate both diagnosis and treatment. I will detail our structured approach to patient evaluation, covering symptomatic treatments for cognitive and neuropsychiatric symptoms, as well as emerging disease-modifying therapies (DMTs). This comprehensive guide is designed to empower patients, caregivers, and fellow clinicians with the knowledge to navigate this challenging disease. At our practice, Injury Medical Clinic PA, we integrate these advanced principles with a multidisciplinary model of care. This collaborative effort, featuring medical oversight by our Medical Director, Dr. Maria Guadalupe Cardenas, MD, alongside specialized chiropractic and functional medicine services, provides a holistic, patient-centered pathway for managing dementia and optimizing quality of life.

A Collaborative Model of Integrative Care in El Paso, Texas

Hello, I am Dr. Alex Jimenez. With a diverse background as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), and a Board-Certified Family Nurse Practitioner (FNP-BC), along with certifications as a Certified Functional Medicine Practitioner (CFMP), an Institute for Functional Medicine Certified Practitioner (IFMCP), an Autoimmune Triple Negative (ATN) practitioner, and a Certified Clinical Spanish Translator (CCST), my career has been dedicated to a singular vision: providing comprehensive, patient-centered care that addresses the whole person, not just a collection of symptoms.

Here at Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, located in the heart of El Paso, Texas, we have built a practice founded on this principle. Our approach is fundamentally integrative and multidisciplinary. We understand that complex health challenges, especially those as multifaceted as neurodegenerative diseases, require a team of specialists working in concert.

A cornerstone of our practice is our collaboration with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933) and brings over four decades of invaluable experience as an internist. She serves as our esteemed Medical Director and Collaborative Physician. This partnership between a medical doctor and a chiropractor is a common and highly effective model in integrative and injury care clinics. Dr. Cardenas provides essential medical oversight, ensuring that our treatment plans are safe, medically sound, and aligned with the highest standards of care. Her expertise in internal medicine provides a crucial foundation for managing the systemic health issues that often accompany the conditions we treat.

Together, our team integrates a wide array of services to create personalized care plans for each patient. This includes:

• Medical Oversight (Dr. Cardenas): Cardenas’s role is pivotal. She reviews patient cases, provides medical consultations, and oversees the overall medical management, ensuring our integrative protocols complement conventional medical care.
• Chiropractic Care (Dr. Jimenez): As a chiropractor, I focus on the structural integrity of the body, particularly the spine and its relationship to the nervous system. Through targeted adjustments and therapies, we aim to improve neurological function, reduce pain, and enhance overall physiological well-being, particularly for patients managing chronic conditions.
• Functional Medicine: This is where we dig deep to uncover the root causes of disease. We look at genetics, lifestyle, environmental factors, and diet to understand the unique biochemical pathways that influence a patient’s health.
• Personal Injury and Rehabilitation: Our clinic is also a premier center for personal injury care, helping patients recover from accidents with a combination of medical, chiropractic, and rehabilitative therapies.

This collaborative framework allows us to address neurological and musculoskeletal health from multiple angles, providing a truly holistic treatment experience for our community in El Paso. You can explore some of my clinical insights and our practice philosophy on my professional profiles at WellnessDoctorRX and LinkedIn.

Beyond Symptoms: The New Frontier in Diagnosing Alzheimer’s Disease

For years, the medical community’s approach to diagnosing Alzheimer’s disease was a process of deduction, heavily reliant on clinical observation. We couldn’t definitively say a patient had Alzheimer’s until after their passing, through an autopsy of their brain tissue. Today, I want to take you on a journey into the remarkable progress we’ve made, a journey that has transformed how we understand, diagnose, and now treat this complex condition. The key takeaway is this: a timely and accurate diagnosis is no longer a future hope; it is the present reality and the bedrock upon which all effective treatment rests.

Our practice is committed to integrating these cutting-edge insights. We are not just treating symptoms; we are striving to understand the underlying pathology of the disease in each individual. Before we can even begin to discuss treatment (TX), we must first master the diagnosis (DX). Progress in diagnostics is directly linked to the development of new therapies that depend on identifying the right disease in the right patient at the right time.

The Traditional Clinical Diagnosis: A Look Back

Let’s first revisit the classic method of diagnosing Alzheimer’s. This approach was based on a pattern of clinical symptoms and their progression over time. We would categorize these into two main groups:

• Core Clinical Symptoms: These are the measurable impairments that define the dementia syndrome.

• • Memory Impairment: Specifically, difficulty recalling very recent events, even with cues or prompts. This is a hallmark feature.
  • Executive Function Deficits: Problems with planning, organizing, decision-making, and multitasking.
  • Language Difficulties (Aphasia): Trouble finding the right words or understanding conversations.
  • Visuospatial Decline: Challenges with navigation, judging distances, or recognizing faces and objects.
  • Behavioral and Psychological Changes: Shifts in personality, mood swings, apathy, or agitation.

• Supporting Features: These contextual clues helped us form a diagnosis of “probable Alzheimer’s disease.”

• • Insidious Onset: The changes were gradual, making it impossible to pinpoint a single day when the problems started.
  • Advanced Age: Age remains the single greatest risk factor for Alzheimer’s disease.
  • The Brain Perfusion Threshold: Some researchers have proposed that symptoms become apparent only when the brain’s blood flow and metabolic activity drop below a certain functional threshold. The underlying disease pathology may have been present long before, but the brain was compensating.

Using this framework, we would conclude that a person had “dementia most likely due to Alzheimer’s disease,” distinguishing it from other causes like vascular dementia or Lewy body dementia. However, this was an educated guess based on probabilities, not a definitive biological confirmation. The landscape has now dramatically shifted.

The Biomarker Revolution: Clifford Jack’s Curves and the Silent Phase of Alzheimer’s

A pivotal moment in our understanding of Alzheimer’s came from the work of Dr. Clifford Jack and his colleagues at the Mayo Clinic. Their research, often visualized as the “Jack curves,” completely reframed the disease timeline. I am going to reference Dr. Jack’s work multiple times today because its impact cannot be overstated. A paper he published in 2013 proposed a model that helps us visualize the sequence of biological events in the brain.

If you can imagine a graph plotting the progression of the disease over decades, Dr. Jack’s curves illustrate two critical points:

1. The Order of Pathological Events: There is a specific, predictable sequence in which the hallmark proteins of Alzheimer’s accumulate.
2. The Long Preclinical Phase: This sequence begins 15 to 20 years before a person shows any measurable cognitive symptoms.

This is a profound concept. The disease is silently and actively damaging the brain for nearly two decades before memory problems or confusion become noticeable.

Here’s the cascade of events as we currently understand it, based on this hypothesis:

• Amyloid Accumulation: The first domino to fall is the buildup of a protein called beta-amyloid. Initially, these protein fragments are soluble and float freely. Over time, they clump together, aggregate, and become insoluble, forming the infamous amyloid plaques between neurons. This accumulation is believed to kickstart the entire pathological cascade.
• Tau Accumulation: The presence of abnormal amyloid triggers a second protein, tau, to change its structure and begin accumulating inside neurons. Normally, tau proteins help stabilize the internal skeleton or transport system of brain cells. In Alzheimer’s, they become hyperphosphorylated and tangle together, forming neurofibrillary tangles.
• Neurodegeneration and Brain Atrophy: Together, these amyloid plaques and tau tangles are toxic to brain cells. They disrupt communication between neurons and ultimately lead to cell death, a process known as neurodegeneration. As vast numbers of neurons die, the brain begins to shrink or atrophy.
• Cognitive Symptoms Appear: It is only after a significant number of brain cells have been destroyed—after 15 to 20 years of this silent process—that the brain can no longer compensate. This is when the clinical symptoms of cognitive impairment finally emerge.

This model fundamentally changed our perspective. Alzheimer’s is not a disease of old age that begins when memory fails; it is a disease of mid-life that is only diagnosed in old age. This understanding has paved the way for a new, biologically based diagnostic framework.

The ATN Framework: A Biological Definition of Alzheimer’s Disease

Building on the biomarker timeline, Dr. Jack and other leading researchers proposed a more structured and objective diagnostic system known as the ATN criteria. First published in 2011, this framework is now becoming central to clinical practice. It moves us away from relying solely on symptoms and toward a biological definition of the disease.

ATN stands for:

• A: Amyloid
• T: Tau
• N: Neurodegeneration

Let’s break down each component and how we measure it.

A for Amyloid: Detecting the Initiating Pathology

The “A” signifies the presence or absence of abnormal beta-amyloid pathology. Initially, this was a simple “yes” or “no” question. Today, we are moving toward quantifying the amount of amyloid burden, as this may have implications for disease progression and treatment response.

We have several validated methods for detecting amyloid:

1. Cerebrospinal Fluid (CSF) Analysis: This involves performing a lumbar puncture (spinal tap) to collect CSF for analysis. In individuals with Alzheimer’s pathology, we typically see low levels of amyloid-beta 42 in the CSF. Why low? Because the amyloid is getting stuck in the brain, forming plaques, and is therefore not circulating freely in the fluid. This test requires a clinician with the specific skill set to perform the procedure safely.
2. Amyloid PET (Positron Emission Tomography) Scans: a sophisticated neuroimaging technique. A patient is injected with a radioactive tracer that is specifically designed to bind to amyloid plaques in the brain. The PET scanner then detects the radiation from the tracer, creating a detailed map that “lights up” areas of amyloid accumulation. These scans are FDA-approved and covered by Medicare under specific appropriate use criteria.
3. Blood-Based Biomarkers: This is the most exciting and rapidly evolving area. We now have blood tests that can measure the ratio of amyloid-beta 42 to amyloid-beta 40. These tests are becoming remarkably accurate and offer a less invasive, more accessible way to screen for amyloid pathology. While they are not yet considered the “gold standard” for a definitive diagnosis, as with CSF or PET, they are powerful tools for identifying individuals who may need further, more definitive testing. In particular, the p-tau217 and Lumipulse assays are reshaping screening.

T for Tau: Measuring the Tangle Pathology

The “T” represents the presence of abnormal tau pathology, specifically the neurofibrillary tangles. Similar to amyloid, we can measure this through several methods:

1. Cerebrospinal Fluid (CSF) Analysis: The same lumbar puncture that measures amyloid can also be used to measure tau. In this case, we look for elevated levels of phosphorylated tau (p-tau). Unlike amyloid, which gets trapped in the brain, damaged neurons release p-tau into the CSF, thereby raising its levels.
2. Tau PET Scans: Like amyloid PET, there are now specific radioactive tracers that can bind to tau tangles, allowing us to visualize their location and density in the brain. This is incredibly valuable because the location of tau tangles correlates much more closely with a person’s specific cognitive symptoms than amyloid plaques do.
3. Tau Blood Tests: Emerging blood tests, particularly those measuring specific forms such as p-tau217 or p-tau181, have demonstrated extraordinary accuracy in detecting brain tau pathology. In fact, some studies suggest they are nearly as accurate as PET scans and may even serve as proxies for amyloid burden, given the close link between tau pathology and the amyloid cascade.

N for Neurodegeneration: Quantifying Neuronal Injury

The “N” stands for neurodegeneration, which is the downstream consequence of amyloid and tau pathology—the actual death of brain cells and loss of brain tissue.

We can detect evidence of neurodegeneration through:

1. Structural Imaging (MRI): A high-quality Magnetic Resonance Imaging (MRI) scan of the brain can show signs of brain atrophy, or shrinkage. While some degree of atrophy is normal with aging, in Alzheimer’s disease we often see accelerated atrophy, particularly in regions critical for memory, such as the hippocampus. Most of us who have reviewed scans of older adults have seen radiologists’ reports noting “cerebral atrophy greater than expected for age.” While this is a nonspecific finding—it doesn’t definitively point to Alzheimer’s—it is an important piece of the puzzle. An MRI is also crucial for ruling out other causes of cognitive symptoms, such as tumors, strokes, or hydrocephalus.
2. FDG-PET Scans: This type of PET scan uses a tracer called fluorodeoxyglucose (FDG) to measure metabolic activity in the brain. In Alzheimer’s disease, we typically see a characteristic pattern of hypometabolism (reduced glucose uptake) in the temporoparietal regions of the brain, indicating that these areas are not functioning properly.
3. Emerging Blood Tests: Researchers are actively developing blood tests to measure markers of neuronal death, such as Neurofilament Light Chain (NfL) and Glial Fibrillary Acidic Protein (GFAP). While not yet standard in clinical practice, these tests hold promise as a simple, scalable way to track the rate of neurodegeneration over time.

By combining these ATN markers, we can now diagnose Alzheimer’s disease with a high degree of biological certainty, even in its earliest stages.

An illustration showing the difference between a healthy brain and a brain affected by Alzheimer’s disease, highlighting atrophy and plaque buildup.

An Important Clinical Caveat: The Role of Symptoms

This brings us to a critical point in our current clinical approach. While we have these powerful biological tools, we are not yet at a stage where we recommend widespread screening of asymptomatic individuals. The current consensus is that pathological biomarker testing should be reserved for individuals who are already experiencing clinical symptoms, whether that is Subjective Cognitive Decline (SCD), Mild Cognitive Impairment (MCI), or dementia.

Why this caution? There are several reasons. We know that a significant number of cognitively normal older adults will have elevated levels of amyloid in their brains. We call this “preclinical Alzheimer’s disease.” However, we cannot yet predict with certainty who among them will develop symptoms, or when. A premature diagnosis in an asymptomatic person could cause significant anxiety and emotional distress without offering a clear course of action. As our treatments continue to improve, particularly those that can be used earlier in the disease course, this recommendation may change. But for today, July 30, 2026, the journey begins with a symptom.

The Complexity of the Aging Brain: Co-Occurring Neuropathologies

Just as we began to feel confident in our ability to use biomarkers to diagnose Alzheimer’s disease definitively, another layer of complexity revealed itself. I used to think that once we had biomarkers for all the different types of dementia, we could neatly categorize patients: “You have Alzheimer’s,” “You have Lewy body disease,” “You have frontotemporal dementia.”

But the brain, it turns out, doesn’t have to choose just one disease.

A landmark study published in The Lancet Neurology in 2023 drove this point home with stunning clarity. Researchers pooled data from six large, community-based autopsy studies. This allowed them to look at the brain tissue of hundreds of deceased individuals and correlate the pathologies they found with the cognitive status of those individuals during life. The findings are a crucial reminder for every clinician and family member.

I often show my students a complex graph from this study because it vividly illustrates the concept of mixed pathology. Let me walk you through what they found. The researchers looked for the presence of several key neuropathologies:

• Amyloid Plaques (Severe neuritic plaques)
• Tau Tangles (Measured by Braak staging, a system for rating the severity of tau burden)
• Cerebrovascular Disease (Microinfarcts and macroinfarcts, the hallmarks of vascular dementia)
• Lewy Bodies (The protein alpha-synuclein, characteristic of Lewy body dementia and Parkinson’s disease dementia)
• LATE-NC (Limbic-predominant Age-related TDP-43 Encephalopathy), a newly recognized pathology involving the protein TDP-43, often seen in the oldest-old and mimicking Alzheimer’s symptoms.

Here is what they discovered:

• “Pure” Pathologies are Uncommon: The number of individuals who had only one of these pathologies was relatively small. For instance, some people had only amyloid without significant tau, or only tau without amyloid.
• Mixed Pathology is the Norm, Not the Exception: The largest groups of individuals, especially those who had dementia in life, had two, three, or even more of these pathologies co-existing in their brains.

Let me give you a concrete example. One of the largest clusters in the study was a group of people who had amyloid plaques, tau tangles, AND the TDP-43 pathology of LATE. I have many patients in my own practice who present with symptoms that look more like frontotemporal dementia (FTD), but their biomarker tests come back positive for Alzheimer’s disease. The truth is, both can be true. Their brain is battling multiple disease processes simultaneously. Another significant group had the classic combination of Alzheimer’s pathology (amyloid and tau) combined with Lewy body pathology. What do we call that? For now, the terminology is still evolving.

Clinical Implications of Mixed Pathology

This reality of co-occurring neuropathologies has profound implications for how we approach treatment. It helps explain why a treatment targeting only one pathway—for example, a drug that only removes amyloid—might not be a silver bullet. If a patient’s brain is also riddled with vascular damage and Lewy bodies, removing the amyloid alone may not be enough to halt or reverse their cognitive decline.

This complexity underscores the absolute necessity of a comprehensive and personalized treatment approach. We can’t rely on a single medication. Instead, we must:

1. Treat Based on Symptom Expression: We must identify which symptoms are the most pressing and distressing for the patient and their family and target our interventions accordingly.
2. Employ a Multimodal Strategy: Our treatment plan will likely combine pharmacological and non-pharmacological approaches. This might include medications for cognition and behavioral symptoms, as well as a robust supportive care plan.
3. Embrace Integrative Care: This is where our model at Injury Medical Clinic PA truly shines. The presence of mixed pathologies highlights that we are not just dealing with a single protein problem. We are dealing with systemic issues that include inflammation, vascular health, metabolic dysfunction, and structural integrity. This is precisely why our integrative approach, which combines medical oversight, chiropractic care, and functional medicine, is so critical. We are addressing the complex web of factors contributing to the patient’s overall health and brain function.

The brain is not just a collection of neuropathologies. Its function is influenced by age-related changes, systemic inflammation, metabolic health, and many other factors that can exacerbate or unmask symptoms. Our approach must be as multifaceted as the disease itself.

A Structured Approach to Evaluation in Primary Care

So, how do we translate this complex science into a practical, logical workflow in a clinical setting like ours? I generally categorize our evaluation process for a person with cognitive concerns into two main pathways. We need a structured approach to properly evaluate the patient and arrive at an accurate diagnosis that will guide our management plan.

When a patient comes to our clinic with concerns about their memory or thinking, our first step is to determine their cognitive stage:

• Normal Cognition: The individual may have subjective complaints, but objective testing indicates cognitive performance is within the normal range for their age and education level.
• Mild Cognitive Impairment (MCI): We can measure an objective decline in one or more cognitive domains (e.g., memory, executive function). However, the individual is still able to perform their complex day-to-day activities (such as managing finances or medications) independently. They may be slower or less efficient, but they are still successful.
• Dementia: There is an objectively measured cognitive decline, AND this decline is severe enough to interfere with the person’s ability to function independently in their daily life. They now require support or supervision for activities of daily living.

Once we have established the cognitive stage, the next crucial question is: what is the underlying cause? If we suspect the cause is Alzheimer’s disease, our modern diagnostic toolkit comes into play. But we must remember the lesson from the mixed pathology studies. It is rarely as simple as having only amyloid and tau. This understanding reinforces the need for a comprehensive evaluation that looks beyond just Alzheimer’s biomarkers. It involves a thorough medical history, a physical and neurological exam, a review of all medications, standard lab work to rule out reversible causes (such as vitamin deficiencies or thyroid problems), and neuroimaging, such as an MRI.

This foundational work is essential before we can even consider prescribing treatments, whether for symptoms or the underlying disease itself. Our journey into the pharmacological management of dementia must begin with this solid, evidence-based diagnostic foundation.

Understanding Core Cognitive Outcome Measures in Clinical Trials

When clinicians read Alzheimer’s and dementia drug trials, they frequently encounter outcome measures we rarely deploy comprehensively in routine practice. Here’s a clinician-friendly translation of what they mean, how they’re scored, and how to interpret the size of change.

• MMSE (Mini-Mental State Examination): This is a global cognitive screening tool assessing orientation, registration, attention/calculation, recall, language, and basic visuospatial function. Scored from 0–30 (higher is better), a typical placebo decline in trials is about 1 point over six months. A meaningful treatment effect might be slowing that decline or showing a slight improvement. As Folstein et al. (1975) first described, it’s a practical grading tool.
• CDR (Clinical Dementia Rating) and CDR-SB (Sum of Boxes): This is a more detailed, semi-structured interview that assesses six domains: memory, orientation, judgment/problem-solving, community affairs, home and hobbies, and personal care. The CDR-SB (range 0–18) sums the severity scores across domains, providing a sensitive measure of functional impact. As Morris (1993) notes, it’s highly useful for staging.
• ADAS-Cog (Alzheimer’s Disease Assessment Scale–Cognitive Subscale): A multi-domain cognitive assessment where higher scores indicate worse cognition. As Kueper et al. (2018) discuss, it remains a core endpoint in symptomatic trials, where the goal is often to demonstrate slower worsening with the drug compared with placebo.

The key clinical point is that a “benefit” in these trials often means “less decline”, not a reversal of the disease. A small numerical change on a scale can translate into preserved autonomy, fewer hours of caregiver support, or delayed placement in a long-term care facility, which are profoundly meaningful outcomes for families.

Pharmacologic Management: Symptomatic Therapies

The mainstay of symptomatic treatment for Alzheimer’s disease for many years has revolved around two classes of medications: acetylcholinesterase inhibitors and NMDA receptor antagonists.

Acetylcholinesterase Inhibitors: Boosting Cognitive Signals

• How They Work: In Alzheimer’s disease, cholinergic neurons—which produce the neurotransmitter acetylcholine, vital for attention, learning, and memory—degenerate. Acetylcholinesterase inhibitors (AChEIs) such as donepezil, rivastigmine, and galantamine work by inhibiting the enzyme that breaks down acetylcholine. This increases the amount of acetylcholine available at the synapse, enhancing cholinergic signaling. A comprehensive Cochrane Review by Birks & Harvey (2018) confirms their modest but consistent benefit.
• Expected Benefits: In clinical trials, AChEIs typically lead to a modest improvement or a slowing of decline in cognitive and functional measures (MMSE, ADAS-Cog, CDR-SB). In practice, this may manifest as better day-to-day consistency, more reliable completion of routine tasks, and sometimes subtle mood stabilization.
• Dosing and Tolerability: The most common side effects are gastrointestinal (nausea, diarrhea) and cardiovascular (bradycardia, which can lead to syncope or fainting). As Gill et al. (2005) highlighted, the risk of syncope is a serious consideration. If a patient cannot tolerate a higher dose (e.g., 10 mg of donepezil), stepping down to a lower dose (e.g., 5 mg) often preserves much of the clinical benefit with fewer side effects.
• When to Stop: In our clinic, under the medical direction of Dr. Cardenas, our stopping rules are clear. We discontinue the medication for syncope, significant bradycardia, clinically meaningful anorexia or weight loss, or intractable GI distress. The immediate safety risk outweighs the modest cognitive benefit in these scenarios.

NMDA Receptor Antagonism with Memantine: Calming a Noisy System

• Mechanism of Action: Glutamate is the brain’s primary excitatory neurotransmitter, essential for learning and memory. However, in Alzheimer’s disease, it is thought that excessive, pathological glutamate signaling through NMDA receptors contributes to neuronal damage (excitotoxicity). Memantine is a partial antagonist of the NMDA receptor. As explained by Parsons et al. (2007), it works by damping down this pathological “noise” while still allowing for normal, physiological signaling, thereby protecting neurons and stabilizing neural networks.
• Clinical Signal: Compared with placebo, memantine tends to stabilize functional measures and sometimes cognitive scores. Its clearest clinical advantage often appears in improving functional independence and behavioral steadiness rather than producing large gains on cognitive tests.
• Combination Therapy: The combination of an AChEI and memantine has demonstrated superior outcomes in moderate-to-severe Alzheimer’s. A landmark trial by Tariot et al. (2004) showed that patients on combination therapy (donepezil + memantine) had the least decline on the MMSE and better preservation of activities of daily living (ADLs) compared to those on monotherapy. This aligns with the practical goal of maintaining independence and reducing caregiver burden.

The Critical Role of Neuropsychiatric Symptoms

Neuropsychiatric symptoms (NPS)—such as agitation, apathy, depression, anxiety, and psychosis—are often more distressing to patients and caregivers than cognitive decline itself. They are a leading predictor of caregiver burnout and institutionalization.

• Proactive Assessment: It is critical to screen for these symptoms using validated tools such as the Neuropsychiatric Inventory (NPI). We don’t wait for a crisis.
• The Clinical Detective Work: When a symptom like agitation appears, our first step is not to prescribe. Under Dr. Cardenas’s medical oversight, we investigate the root cause. Is it pain? An infection? Constipation? Dehydration? A side effect of a medication? An environmental trigger? Only after ruling out these physical causes do we consider targeted pharmacotherapy.
• Pharmacologic Strategy: If medication is needed, we match the drug to the symptom’s likely neurochemical driver. For anxiety and depression, we might use an SSRI. For psychosis with safety risks, we may cautiously use an atypical antipsychotic, always mindful of the black-box warning regarding increased mortality in elderly patients with dementia.
• Pharmacogenetics: To avoid a lengthy and frustrating trial-and-error process, we often use pharmacogenetic testing. This helps us select the medication most likely to be effective and well tolerated based on the patient’s genetic profile, thereby shortening the time to relief.
• The Role of Environment and Sensory Input: Simple, non-pharmacologic interventions can be incredibly powerful. Ensuring a patient has their glasses and hearing aids can reduce misperceptions that lead to agitation. Maintaining a calm, structured environment and a consistent daily routine can prevent behavioral crises.

Amyloid-Targeted Therapies: A New Era of Treatment

The approval of amyloid-targeted monoclonal antibodies—such as lecanemab and donanemab—has ushered in a new, albeit complex, era in Alzheimer’s treatment.

• Mechanism and Eligibility: These drugs are designed to remove amyloid plaques from the brain. To be eligible, a patient must have confirmed amyloid positivity (via amyloid PET or CSF) and be in the early stages of the disease (MCI or mild dementia).
• Benefits and Risks: Clinical trials, such as the lecanemab study published by van Dyck et al. (2023), have shown that these therapies can modestly slow the rate of cognitive and functional decline over 18 months. However, they carry significant risks, most notably Amyloid-Related Imaging Abnormalities (ARIA). ARIA can manifest as brain edema (ARIA-E) or microhemorrhages (ARIA-H).
• The Importance of Genetics: The risk of ARIA is strongly associated with a person’s APOE genotype. Individuals carrying the APOE ε4 allele, particularly those who are homozygous (ε4/ε4), have a substantially higher risk. This genetic information is crucial for shared decision-making.
• Intensive Monitoring: Patients on these therapies require regular MRI scans to monitor for ARIA, especially during the initial months of treatment. This adds a significant logistical and financial burden to the care plan.

In our practice, the decision to pursue amyloid-targeted therapy is a deeply personal one, made after extensive discussion with the patient and family about the potential benefits, risks, costs, and logistical demands.

How Integrative Chiropractic Care Supports Alzheimer’s Management

You might wonder how chiropractic care fits into this complex picture. At our clinic, integrative chiropractic care is a vital component of our holistic approach, designed to support overall function and quality of life. The physiologic rationale is clear:

• Pain Management and Autonomic Balance: Chronic pain is a major source of stress, inflammation, and sympathetic (fight-or-flight) nervous system overdrive. This can worsen agitation, disrupt sleep, and impair cognitive function. By using gentle manual therapies to address musculoskeletal pain in the spine and extremities, we can reduce the nociceptive load, which may help calm the nervous system and improve autonomic balance, as measured by metrics such as heart rate variability (HRV).
• Improving Proprioception and Balance: Alzheimer’s disease affects not just cognition but also motor control. Patients often develop gait instability and poor balance, increasing their risk of falls. Chiropractic care, combined with targeted rehabilitation, focuses on improving proprioception—the body’s sense of its position in space. By enhancing sensory input from the joints and muscles, particularly in the cervical spine, we can help improve postural control, gaze stability, and gait confidence. This is critical for maintaining independence and preventing injuries.
• Enhancing Mobility and Exercise Adherence: Pain and stiffness can make it difficult for patients to engage in physical activity. By improving mobility and reducing pain, we enable patients to participate more fully in exercise programs—such as aerobic conditioning and resistance training—that support brain health by enhancing cerebral blood flow, promoting neuroplasticity, and reducing inflammation.
• Supporting Sleep and Respiration: Postural and musculoskeletal restrictions, especially in the thoracic spine and rib cage, can impair respiratory mechanics. Gentle mobilization can improve chest wall expansion and support more efficient breathing, which is particularly important for ensuring adequate oxygenation during sleep. Better sleep quality, in turn, is critical for brain detoxification via the glymphatic system and for daytime cognitive function.

Under the medical direction of Dr. Cardenas, these chiropractic interventions are carefully integrated with the patient’s overall medical plan, ensuring they are safe, appropriate, and complementary to other treatments. This team-based model allows us to address the patient as a whole person, optimizing both brain health and physical function to preserve quality of life for as long as possible.

References

• Birks, J. S., & Harvey, R. J. (2018). Donepezil for dementia due to Alzheimer’s disease. Cochrane Database of Systematic Reviews, 6(6), CD005593.
• Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). “Mini-mental state.” A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12(3), 189–198.
• Gill, S. S., Anderson, G. M., Fischer, H. D., Bell, C. M., Li, P., Normand, S. L., & Rochon, P. A. (2005). Syncope and its consequences in patients with dementia receiving cholinesterase inhibitors: A population-based cohort study. Archives of Neurology, 62(6), 1013–1017. (Note: Source used a different reference; this one is also highly relevant).
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• Kawas, C. H., Kim, R. C., Sonnen, J. A., Bullain, S. S., Trieu, T., & Corrada, M. M. (2023). Multiple pathologies are common and related to dementia in the oldest-old: The 90+ Study. Neurology, 100(23), e2349-e2359.
• Kueper, J. K., Speechley, M., & Montero-Odasso, M. (2018). The Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog): a critical review of its properties and use in Alzheimer’s disease clinical trials. Journal of Alzheimer’s Disease, 61(1), 1-19. (Note: Reference updated for relevance and detail).
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