Connecting the 3 Ps for Alzheimer’s Disease: Pathophysiology, Manifestations, Pharmacology

CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology

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CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology

Instructions: Read the assigned textbook chapters. Choose ONE diagnosis from the list below. Fill out the assignment below by connecting essential knowledge of the pathophysiology of the primary diagnosis/problem to the physical examination, clinical manifestations and to the pharmacotherapies. Think about this as an APRN seeing a patient in clinical practice. Include a relevant diagnostic test and non-pharmacotherapies that could be used related to the pathophysiology of the disease. Show the connection between the pathophysiologic process of the disease, the clinical manifestations and the pharmacotherapeutic treatment and plan.

It is required that at least 3 citations / 3 references are used for this assignment. Points are included into the points listed for each section. A citation is required for the following sections: “Pathophysiology,” “Physical Findings” (Body Systems; Subjective / HPI; Objective); “Labs and Diagnostics,” “Diagnosis” (Pathophysiology of differential diagnoses), and “Pharmacotherapy” (Plan, Guidelines, and SDoH). One reference must be from the Rogers’ Pathophysiology textbook and one citation must be from the most recent clinical practice guidelines for the disease

This assignment is worth 35 points . Please review the rubric for details of point requirements.

DIAGNOSIS CHOSEN FROM THE ONE OF THE DIAGNOSES HERE: ( 1 point)

Dementia / Alzheimer – Older Adult

( It is required that a different population must be chosen for each of the next assignments. For example, if you choose an adult disease for cardiovascular system, then you should choose a pediatric disease for pulmonary assignment and then choose women’s health for GI assignment).

Diagnosis: Dementia / Alzheimer – Older Adult

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY OF PRIMARY MEDICAL CONCERN (Disease chosen – specific to the population) (4 points)

(100-200 WORDS)

Alzheimer’s disease (AD) is caused by the gradual buildup of protein aggregation and lesions or blisters from abnormal protein accumulation that damage the neurons and leave the patient with cognitive deficits and practical issues (Kumar et al., 2024). The hallmark pathological features include extracellular accumulation of beta-amyloid (Aβ) plaques due to impaired clearance and intracellular neurofibrillary tangles composed of hyperphosphorylated tau proteins. These changes impact brain cell signaling, prevent brain cell connections, and kill brain cells. Chronic neuroinflammation, which is caused by active microglia and astrocytes, worsens the breakdown of neurons and makes the disease progress faster. Mutations in the APOE-ε4 allele increase risk due to genetic factors, while age is the strongest risk factor (Serrano-Pozo et al., 2021). The disease causes degeneration of cholinergic neurons in the basal forebrain, which progressively declines the level of acetylcholine. This contributes to Alzheimer’s disease-related cognitive impairment, memory loss, language problems, and executive dysfunction. As the disease progresses, the cortex shrinks and the brain ventricles expand. There is also a loss of global cerebral volume, which is commonly observed in older adults

PHYSICAL FINDINGS

BODY SYSTEMS THAT ARE DIRECTLY IMPACTED BY THIS MEDICAL PROBLEM (3 points)

EXPLAIN HOW EACH SYSTEM YOU CHOSE IS AFFECTED – IT CAN BE A POSSIBLE COMPLICATION OF THE DISEASE. (Ex. Integumentary affected from diabetes related to a diabetic wound OR Neurologic system affected by diabetes related to vision changes). ( Minimum 3 body systems )

Neurologic System

Alzheimer’s disease primarily affects the neurologic system through progressive neuronal loss and synaptic dysfunction. The accumulation of beta-amyloid plaques and tau tangles leads to cortical atrophy, especially in the hippocampus and frontal lobes. This results in hallmark symptoms such as memory impairment, executive dysfunction, disorientation, language difficulties, and, in later stages, behavioral disturbances including agitation and hallucinations (El Haj et al., 2020). Neurologic decline is the most direct and central impact of the disease.

Cardiovascular System

Vascular health plays a crucial role in Alzheimer’s progression. Cerebral hypoperfusion from microvascular damage or coexisting conditions such as hypertension and atherosclerosis worsens neuronal injury. According to Papadopoulou et al. (2025), patients with Alzheimer’s often develop autonomic dysfunction, leading to blood pressure variability, cardiac arrhythmias, and increased fall risk due to orthostatic hypotension. In addition, cardiovascular comorbidities increase the risk of mixed dementia, which complicates treatment and outcomes.

Gastrointestinal System

The gastrointestinal system can be indirectly affected by Alzheimer’s disease due to both neurological decline and pharmacologic treatment. Progressive cognitive decline leads to dysphagia, anorexia, and impaired nutritional intake, increasing the risk for malnutrition and aspiration pneumonia (Mira et al., 2022). Cholinesterase inhibitors, a mainstay of treatment, frequently cause gastrointestinal side effects such as nausea, vomiting, diarrhea, and weight loss. These complications further compromise the patient’s overall health status.

PRIORITY SUBJECTIVE SYMPTOMS / HISTORY OF PRESENT ILLNESS (HPI)

(on SOAP notes – the S stands for subjective – which is information from the patient)

Align the subjective symptoms to the pathophysiology of the disease. These are the things that a patient may tell you if they have the disease. (2 points)

THESE ARE THE SYMPTOMS (Information obtained from the patient about the problem)

O nset: Patient reports gradual memory loss beginning approximately 2–3 years ago, initially with forgetting recent conversations and misplacing items.

L ocation: Cognitive decline is most noticeable in memory and thinking; patient describes difficulty recalling names, managing finances, and following conversations.

D uration: Symptoms have been persistent and progressively worsening over time, with increasing interference in daily functioning.

C haracteristics: Family notes confusion about time and place, repeated questioning, word-finding difficulties, and changes in mood (irritability and anxiety). Patient also describes difficulty with problem-solving and occasionally forgetting familiar routes when driving.

A ggravating factors: Symptoms worsen with fatigue, stress, and unfamiliar environments.

R elieving factors: Short-term improvement noted with rest and reassurance from caregivers; structured routines at home reduce confusion.

T reatments: Patient has not tried medications yet but has been using memory aids (sticky notes, phone reminders) with limited success.

S everity: Patient rates memory loss as “very frustrating” and reports significant impact on independence. Family members report increased concern for safety and inability to manage complex daily tasks. CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology – Alzheimer’s disease

PRIORITY PHYSICAL EXAMINATION

OBJECTIVE SYMPTOMS (3 points)

(on SOAP notes – the O stands for objective – which is information from the provider)

Align the examination / findings to the body systems that affected. ( Minimum 3 systems )

You should build a “clinical picture” for each symptom to start ruling in or out diagnoses. In other words, viral pharyngitis vs strep vs tonsillitis vs epiglottitis, etc.

THESE ARE THE SIGNS (Information the provider actually assesses during the physical examination relevant to the problem)

General: Patient appears well-nourished but mildly disoriented to time and place; cooperative but with intermittent anxiety; grooming somewhat neglected.

HEENT: No acute abnormalities; pupils equal and reactive, extraocular movements intact; mild difficulty following multi-step commands noted during exam.

Hematologic: No pallor, bruising, or lymphadenopathy; no evidence of anemia or bleeding disorders.

Cardiac: Regular rate and rhythm; no murmurs, rubs, or gallops; mild orthostatic hypotension observed, consistent with autonomic dysfunction often associated with advanced neurocognitive disorders.

Respiratory: Lungs clear bilaterally; no adventitious sounds; normal respiratory effort.

Endocrine: No thyromegaly or nodules; no tremors; blood glucose within normal limits; helps rule out thyroid dysfunction or diabetes as contributors to cognitive impairment.

GI: Abdomen soft, non-tender; normal bowel sounds; mild weight loss reported, likely due to decreased appetite and early dysphagia.

GU: No suprapubic tenderness; continent but patient may note occasional urinary incontinence during nighttime, consistent with advanced cognitive decline.

Musculoskeletal: Mild shuffling gait and unsteadiness observed, consistent with late-stage disease and increased fall risk.

Integumentary: Skin warm, intact; no rashes or lesions; mild dryness noted.

Extremities: No edema; peripheral pulses intact; fine motor coordination reduced (difficulty buttoning shirt during exam).

MAKING THE CONNECTION:

Patho-Clinical Manifestations

Write a paragraph explaining how the subjective and objective findings are linked to the pathophysiology of the disease. (150-300 words) (3 points)

Alzheimer’s disease is driven by the accumulation of beta-amyloid plaques, tau neurofibrillary tangles, neuronal apoptosis, and synaptic dysfunction, which collectively impair neurotransmission and lead to cortical atrophy (Kumar et al., 2024). These underlying pathophysiological changes explain the patient’s subjective complaints of gradual memory loss, disorientation, word-finding difficulties, and difficulty managing daily tasks. Progressive hippocampal damage disrupts short-term memory consolidation, while cortical involvement contributes to impaired judgment, language deficits, and executive dysfunction, consistent with the patient’s frustration and increasing dependence. The patient’s report of symptoms worsening with fatigue and unfamiliar environments reflects the brain’s diminished cognitive reserve, making compensatory processes less effective under stress. Objective findings also align with this pathophysiology: disorientation to time and place and difficulty following multi-step commands correspond to impaired cortical processing, while shuffling gait and mild unsteadiness may result from neuronal degeneration extending to motor pathways. Autonomic dysfunction, manifesting as orthostatic hypotension, is explained by cholinergic neuron loss in the basal forebrain and brainstem. Gastrointestinal changes such as weight loss and early dysphagia are secondary to cortical decline affecting feeding behaviors and neuromuscular coordination, in addition to side effects of cholinesterase inhibitors in treated patients.

LABS / DIAGNOSTIC TESTING

LAB AND DIAGNOSTIC FINDINGS THAT MAY BE ABNORMAL (2 points)

List the appropriate tests / labs (minimum 2) and explain the normal / abnormal result and how the lab test helps the APRN differentiate this diagnosis from others on the differential list.

Neurocognitive Testing (MoCA or MMSE):

Normal result : Score ≥ 26 (MoCA) or ≥ 24 (MMSE) indicates intact cognition.

Abnormal result : Alzheimer’s patients typically score below these cutoffs, with prominent deficits in short-term memory, orientation, and executive function. These tools help differentiate Alzheimer’s disease from mild cognitive impairment (MCI) or normal age-related changes, where memory lapses are less severe and daily functioning remains preserved (Boer et al., 2025).

MRI of the Brain:

Normal result : Symmetrical brain structures with no significant cortical atrophy or ventricular enlargement.

Abnormal result : Generalized cortical atrophy, particularly in the hippocampus and temporal-parietal regions, with compensatory ventricular enlargement. MRI helps rule out other causes of cognitive decline such as vascular dementia (multiple infarcts), brain tumors, or normal-pressure hydrocephalus (ventriculomegaly without atrophy) (Wang et al., 2020).

Laboratory Workup (TSH, Vitamin B12, CBC, CMP):

Normal result : Values within reference range, excluding reversible causes of dementia.

Abnormal result : Hypothyroidism (low TSH, low T4) or Vitamin B12 deficiency (low serum B12, elevated methylmalonic acid) can mimic Alzheimer’s-like symptoms. CBC and CMP may reveal anemia, electrolyte imbalances, or renal/hepatic dysfunction contributing to confusion. These labs are essential to differentiate Alzheimer’s from metabolic or endocrine causes of cognitive impairment (Maneval et al., 2022). CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology – Alzheimer’s disease

MAKING THE CONNECTION:

Patho-Diagnostic Tests / Labs (3 points)

Write a paragraph explaining how the labs and/or diagnostic tests are linked to the pathophysiology of the disease. (150 – 300 words)

The diagnostic evaluation of Alzheimer’s disease directly reflects its underlying pathophysiology. Neurocognitive assessments such as the Mini-Mental State Examination (MMSE) or Montreal Cognitive Assessment (MoCA) measure deficits in memory, orientation, attention, and executive functioning, which stem from neuronal loss and synaptic dysfunction in the hippocampus and cortical regions. These deficits correlate with the disease’s pathologic hallmarks: beta-amyloid deposition and tau-related neurofibrillary tangles, which disrupt neuronal communication and lead to cortical atrophy (Kumar et al., 2024). Neuroimaging with MRI provides further structural evidence of this degeneration, often showing hippocampal and temporal-parietal atrophy with ventricular enlargement (Kim et al., 2022). These imaging changes directly mirror the areas most affected by abnormal protein aggregation and neuroinflammation. Laboratory studies, such as thyroid-stimulating hormone (TSH) and vitamin B12, are essential to rule out reversible causes of dementia that mimic Alzheimer’s symptoms. For example, hypothyroidism can impair neuronal metabolism, while vitamin B12 deficiency causes demyelination and neuronal dysfunction, conditions that present with similar cognitive decline but have distinct pathophysiologic origins (Nawaz et al., 2020). A complete blood count (CBC) and metabolic panel can also identify anemia, electrolyte disturbances, or hepatic and renal dysfunction that may worsen confusion. Therefore, the integration of cognitive testing, imaging, and laboratory evaluation creates a comprehensive diagnostic picture. Cognitive and imaging findings confirm the neurodegenerative pathology characteristic of Alzheimer’s, while laboratory studies differentiate it from metabolic, endocrine, or vascular causes, ensuring diagnostic accuracy and appropriate treatment planning.

DIFFERENTIAL DIAGNOSIS

2 POSSIBLE DIFFERENTIAL DIAGNOSES (DD) (1 point)
1. Vascular Dementia

2. Lewy Body Dementia

EXPLAIN THE PATHOPHYSIOLOGY OF THE 2 DIFFERENTIAL DIAGNOSES AND WHY THEY CAN BE RULED OUT

(2 points)

1. Pathophysiology: Vascular dementia results from reduced cerebral blood flow due to multiple infarcts, chronic ischemia, or microvascular disease. The ischemic injury leads to neuronal death, white matter changes, and stepwise declines in cognitive function (Uwagbai & Kalish, 2023). Symptoms often include slowed processing, impaired executive function, and focal neurologic deficits depending on infarct location.

Why ruled out : In this case, MRI findings show diffuse cortical atrophy in the hippocampal and temporal lobes rather than evidence of multiple infarcts or white matter lesions. In addition, the patient’s history suggests a gradual and progressive decline rather than a stepwise deterioration, making vascular dementia less likely.

2. Pathophysiology: Lewy Body Dementia (LBD) is caused by abnormal alpha-synuclein protein deposition (Lewy bodies) in cortical and subcortical neurons (Liang et al., 2025). This disrupts dopaminergic and cholinergic signaling, leading to a triad of fluctuating cognition, visual hallucinations, and parkinsonian motor symptoms. Autonomic dysfunction is also common.

Why ruled out: The patient does not report recurrent visual hallucinations, fluctuating alertness, or significant parkinsonism (e.g., resting tremor, rigidity). Instead, the predominant clinical picture involves progressive memory impairment and disorientation, which aligns more closely with Alzheimer’s pathophysiology. Neuroimaging also does not show the basal ganglia involvement typically associated with LBD.

PHARMACOTHERAPY / NON-PHARMACOTHERAPY / PLAN

PLAN

(on SOAP notes – the P stands for plan)

(4 points)

MEDS:

· Initiate Donepezil 5 mg PO daily (cholinesterase inhibitor) to enhance cholinergic transmission and slow cognitive decline (Alzheimer’s Association, 2024).

· Consider Memantine 5 mg PO daily if disease progresses to moderate-to-severe stage, targeting NMDA receptor-mediated excitotoxicity.

· Avoid anticholinergic medications, which can worsen cognitive impairment (Chatterjee et al., 2021).

FURTHER TESTING:

· MRI brain to evaluate extent of cortical atrophy and rule out other structural causes (e.g., vascular lesions, tumors, hydrocephalus).

· Routine labs annually (CBC, CMP, TSH, Vitamin B12) to monitor for reversible causes of cognitive changes or comorbid conditions.

· Cognitive reassessment every 6–12 months using MoCA or MMSE to track disease progression.

EDUCATION:

Disease: Educate patient and family about Alzheimer’s as a progressive neurodegenerative condition, expected symptom trajectory, and the importance of safety planning.

Meds: Explain purpose of cholinesterase inhibitors (symptom management, not cure), common side effects (GI upset, bradycardia, dizziness), and importance of adherence.

Lifestyle Changes: Encourage a Mediterranean diet rich in fruits, vegetables, whole grains, and omega-3 fatty acids, which supports vascular and brain health. Recommend regular aerobic and strength-training exercises (30 minutes, 5 days/week) to enhance cognition and reduce cardiovascular risk. Promote cognitive stimulation (puzzles, reading, social activities) and structured daily routines to minimize confusion.

FOLLOW-UP:

Schedule follow-up in 6 weeks to evaluate medication tolerance and side effects.

Continue follow-ups every 3–6 months for medication adjustments, safety evaluations, and caregiver support.

Discuss advanced care planning, support groups, and community resources to address caregiver burden and long-term planning.

CLINICAL GUIDELINE FOR THIS DISEASE: (2 point)

Look up the most recent clinical guidelines of the disease you have chosen and add the link to the guidelines here.

Alzheimer’s Association. (2024). Clinical practice guidelines & evidence . Alzheimer’s Disease and Dementia. https://www.alz.org/professionals/health-systems-medical-professionals/clinical-practice-guidelines-and-evidence

Palmqvist, S., Whitson, H. E., Allen, L. A., Suarez‐Calvet, M., Galasko, D., Karikari, T. K., Okrahvi, H. R., Paczynski, M., Schindler, S. E., Teunissen, C. E., Zetterberg, H., Carrillo, M. C., Edelmayer, R. M., Mahinrad, S., McAteer, M. B., Kahale, L. A., Pahlke, S., & Tampi, M. P. (2025). Alzheimer’s association clinical practice guideline on the use of blood‐based biomarkers in the diagnostic workup of suspected Alzheimer’s disease within specialized care settings. Alzheimer’s & Dementia , 21 (7). https://doi.org/10.1002/alz.70535

MAKING THE CONNECTION:

Patho-Pharm (3 points)

Write a paragraph explaining how the pharmacotherapy (medications) is linked to the pathophysiology of the disease. (150-300 words)

Pharmacologic therapy for Alzheimer’s disease is directly targeted at mitigating the neurotransmitter deficits and excitotoxic processes caused by the disease’s underlying pathophysiology. One of the central features of Alzheimer’s is the degeneration of cholinergic neurons in the basal forebrain, leading to decreased acetylcholine levels and impaired synaptic transmission, which manifest as memory loss, impaired learning, and cognitive decline. Cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine act by inhibiting acetylcholinesterase, the enzyme responsible for breaking down acetylcholine in the synaptic cleft (Singh & Sadiq, 2023). These agents partially compensate for the loss of cholinergic neurons and enhance cognitive function, attention, and memory in patients by increasing the availability of acetylcholine. In moderate to severe Alzheimer’s, memantine, an NMDA receptor antagonist, is added to treatment. Alzheimer’s pathology involves excess glutamate release and NMDA receptor overstimulation, which causes excitotoxicity and neuronal apoptosis. Memantine regulates glutamatergic signaling by preventing prolonged calcium influx into neurons, thereby reducing neurotoxicity while still allowing normal neurotransmission necessary for learning and memory (Kuns et al., 2024). These medications do not cure the disease or halt the accumulation of beta-amyloid plaques and tau tangles but instead provide symptomatic relief by targeting the neurochemical disruptions caused by these pathological processes.

SOCIAL DETEREMINANTS OF HEALTH (SDoH) (2 points)

Identify one SDoH that could affect a patient with this disease. Explain how it would affect the individual and the disease process AND explain your plan – as the provider – to maneuver treatment with the SDoH concern . (150-300 words)

One important social determinant of health (SDoH) that significantly affects patients with Alzheimer’s disease is socioeconomic status, particularly financial strain and limited access to care. Alzheimer’s disease is a chronic, progressive condition that requires frequent medical follow-up, costly pharmacologic therapy, and extensive caregiver support. Patients from lower-income households may face difficulty affording medications such as cholinesterase inhibitors or memantine, limiting their ability to maintain consistent symptom management. Financial hardship also contributes to delayed diagnosis, reduced access to neuroimaging and specialist care, and limited availability of community-based support services (Monfared et al., 2022). These barriers exacerbate disease progression by leaving patients without adequate interventions or resources to optimize safety, nutrition, and cognitive stimulation. For example, my plan would involve tailoring treatment to the patient’s financial and social context. For instance, I would prioritize prescribing generic formulations of medications when available, connect the family to pharmaceutical assistance programs, and provide referrals to community resources such as the Alzheimer’s Association for support groups, respite care, and education. In addition, I would work with case management and social work teams to explore home health services and caregiver training options that can be accessed at reduced or no cost. Addressing socioeconomic barriers in a proactive, resource-oriented way ensures that patients with Alzheimer’s disease receive equitable care, even when financial constraints could otherwise limit adherence and worsen disease outcomes (Alzheimer’s Association, 2024). CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology – Alzheimer’s disease

THIS ASSIGNMENT ALIGNS WITH THE FOLLOWING COURSE OBJECTIVES:

1.Apply the model of homeostasis to the understanding of the theoretical/empirical basis of physiologic regulation and pathophysiologic phenomena of the human body

Describe abnormal physiological disorders in the human population.

Examine the interaction between genetics and environmental factors in the development of a given disorder

Distinguish the signs, symptoms, and diagnostic test results associated with disorders affecting the human population

Integrate the cultural, socioeconomic, gender, and age-related differences in the pathophysiologic response and treatment associated to disease or injury.

CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology – Alzheimer’s disease

6.Interpret physiologic function and pathophysiologic dysfunction in the context of preparing to make competent clinical decisions in an advanced practice role

References

Alzheimer’s Association. (2024a). Clinical practice guidelines & evidence . Alzheimer’s Disease and Dementia. https://www.alz.org/professionals/health-systems-medical-professionals/clinical-practice-guidelines-and-evidence

Alzheimer’s Association. (2024b). Management . Alzheimer’s Disease and Dementia. https://www.alz.org/professionals/health-systems-medical-professionals/management

Boer, L. de, Poos, J. M., Van, E., F.H, J., Swartenbroekx, T., Dopper, E. G. P., Boesjes, P., Tahboun, N., Bouzigues, A., Foster, P. H., Ferry-Bolder, E., Adams-Carr, K., Russell, L. L., Convery, R. S., Rohrer, J. D., Seelaar, H., & Jiskoot, L. C. (2025). Montreal cognitive assessment vs the Mini-mental state examination as a screening tool for patients with genetic frontotemporal dementia. Neurology , 104 (5). https://doi.org/10.1212/wnl.0000000000213401

Chatterjee, S., Bali, V., Carnahan, R. M., Chen, H., Johnson, M. L., & Aparasu, R. R. (2021). Anticholinergic burden and risk of cognitive impairment in elderly nursing home residents with depression. Research in Social and Administrative Pharmacy . https://doi.org/10.1016/j.sapharm.2019.05.020

El Haj, M., Badcock, J. C., & Larøi, F. (2020). Hallucinations and source monitoring in Alzheimer’s disease. Cognitive Neuropsychiatry , 25 (6), 435–446. https://doi.org/10.1080/13546805.2020.1832457

Kim, J., Jeong, M., Stiles, W. R., & Choi, H. S. (2022). Neuroimaging modalities in Alzheimer’s disease: Diagnosis and clinical features. International Journal of Molecular Sciences , 23 (11), 6079. https://doi.org/10.3390/ijms23116079

Kumar, A., Tsao, J. W., Sidhu, J., & Goyal, A. (2024, February 12). Alzheimer disease . National Library of Medicine; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK499922/

Kuns, B., Rosani, A., & Varghese, D. (2024). Memantine . National Library of Medicine; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK500025/

Liang, J., Li, R., Wong, G., & Huang, X. (2025). Lewy body dementia: Exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein. Molecular Neurodegeneration , 20 (1). https://doi.org/10.1186/s13024-025-00879-0

Maneval, J., Woods, J. K., Feany, M. B., Miller, M. B., Silbersweig, D. A., Gale, S. A., Daffner, K. R., & McGinnis, S. M. (2022). Case study 3: A 58-year-old woman referred for evaluation of suspected Alzheimer dementia. The Journal of Neuropsychiatry and Clinical Neurosciences , 34 (4), 307–315. https://doi.org/10.1176/appi.neuropsych.20220113

Mira, A., Gonçalves, R., & Rodrigues, I. T. (2022). Dysphagia in Alzheimer’s disease: A systematic review. Dementia & Neuropsychologia , 16 (3). https://doi.org/10.1590/1980-5764-dn-2021-0073

Monfared, A. A. T., Byrnes, M. J., White, L. A., & Zhang, Q. (2022). The humanistic and economic burden of Alzheimer’s disease. Neurology and Therapy , 11 . https://doi.org/10.1007/s40120-022-00335-x

Nawaz, A., Khattak, N. N., Khan, M. S., Nangyal, H., Sabri, S., & Shakir, M. (2020). Deficiency of vitamin B12 and its relation with neurological disorders: A critical review. The Journal of Basic and Applied Zoology , 81 (1). https://doi.org/10.1186/s41936-020-00148-0

Palmqvist, S., Whitson, H. E., Allen, L. A., Suarez‐Calvet, M., Galasko, D., Karikari, T. K., Okrahvi, H. R., Paczynski, M., Schindler, S. E., Teunissen, C. E., Zetterberg, H., Carrillo, M. C., Edelmayer, R. M., Mahinrad, S., McAteer, M. B., Kahale, L. A., Pahlke, S., & Tampi, M. P. (2025). Alzheimer’s association clinical practice guideline on the use of blood‐based biomarkers in the diagnostic workup of suspected Alzheimer’s disease within specialized care settings. Alzheimer’s & Dementia , 21 (7). https://doi.org/10.1002/alz.70535

Papadopoulou, M., Stefanou, M.-I., Bakola, E., Moschovos, C., Athanasaki, A., Tsigkaropoulou, E., Michopoulos, I., Paraskevas, G. P., Gournellis, R., & Tsivgoulis, G. (2025). Dysautonomia in Alzheimer’s disease: A systematic review. Brain Sciences , 15 (5), 502–502. https://doi.org/10.3390/brainsci15050502

Serrano-Pozo, A., Das, S., & Hyman, B. T. (2021). APOE and Alzheimer’s disease: Advances in genetics, pathophysiology, and therapeutic approaches. The Lancet Neurology , 20 (1), 68–80. https://doi.org/10.1016/s1474-4422(20)30412-9

Singh, R., & Sadiq, N. M. (2023, July 17). Cholinesterase inhibitors . National Library of Medicine; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK544336/

Uwagbai, O., & Kalish, V. B. (2023, October 22). Vascular dementia . PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK430817/

Wang, Q., He, C., Zhu, Y., Zhang, Q., Zhang, Z., & Xie, C. (2020). Cortical atrophy mediates the accumulating effects of vascular risk factors on cognitive decline in the Alzheimer’s disease spectrum. Aging , 12 (14), 15058–15076. https://doi.org/10.18632/aging.103573 CONNECTING THE 3 Ps: Pathophysiology, Physical Manifestations, Pharmacology – Alzheimer’s disease