Dementia Case Study

Abstract

Dementia describes a spectrum of progressive neurodegenerative disorders that impair memory, thinking, behaviours and the ability to perform activities of daily living. Alzheimer’s disease (AD) accounts for roughly two‑thirds of dementia cases[1]. Global estimates indicate that more than 55 million people were living with dementia in 2021 and over 10 million new cases occur annually[2]. The economic burden is enormous; in 2019 the global cost of dementia exceeded US$ 1.3 trillion[3]. This case study explores the pathophysiology and risk factors of dementia, outlines diagnostic assessment and evidence‑based management, and presents a fictional case to illustrate the complexities of care. Emphasis is placed on nursing management, interprofessional collaboration and palliative care considerations.

Introduction

Dementia is an umbrella term describing a decline in cognitive ability severe enough to interfere with daily life[4]. It is not a normal part of ageing but is strongly age‑associated; prevalence approximately doubles every 5 years after age 65[5]. Alzheimer’s disease, the most common form, is characterized by insidious onset and progressive impairment of memory, language, reasoning and executive function[1]. Vascular dementia, dementia with Lewy bodies, frontotemporal lobar degeneration and other etiologies contribute to the remaining cases[6].

According to the World Health Organization (WHO), dementia is the seventh leading cause of death worldwide and one of the major causes of disability and dependency among older people[7]. Over 60 % of individuals with dementia live in low‑ and middle‑income countries[2]. By 2030 the number of people living with dementia is expected to reach 78 million and by 2050 nearly 139 million[8]. The direct medical costs account for only about 20 % of total dementia costs; most expenses arise from informal and social care[9].

Although age and genetics are important determinants, approximately 40 % of dementia cases may be attributable to modifiable risk factors such as hypertension, diabetes, obesity, depression, smoking, physical inactivity and social isolation[10]. Recognizing and addressing these factors present opportunities for prevention and early intervention. Timely diagnosis is crucial to allow persons with dementia and their families to plan care, access support services and participate in decisions. Nurses play a pivotal role in assessment, management, caregiver support and coordination of palliative care. The following sections summarize the pathophysiology, risk factors, clinical manifestations, assessment, management and nursing considerations of dementia and then apply these concepts to a comprehensive case study.

Pathophysiology and Etiology

Neuropathological hallmarks

The neuropathological signature of AD includes extracellular amyloid‑β (Aβ) plaques and intracellular neurofibrillary tangles composed of hype phosphorylated tau protein[11]. Two major hypotheses explain these changes:

Cholinergic hypothesis: Degeneration of cholinergic neurons in the basal forebrain and neocortex leads to reduced levels of acetylcholine. Anticholinergic drugs exacerbate cognitive impairment. Aβ accumulation is thought to cause cholinergic synaptic loss and impaired neurotransmitter release[12].
Amyloid cascade hypothesis: Abnormal processing of amyloid precursor protein (APP) by β‑ and γ‑secretases generates Aβ peptides, particularly the neurotoxic Aβ42 fragment[13]. Aβ42 aggregates into fibrils, forming plaques that trigger neuroinflammation, oxidative stress and synaptic dysfunction[13].

Genetic factors contribute to pathogenesis. Mutations in the APP gene on chromosome 21, presenile 1 (PSEN1) on chromosome 14 and presenilin 2 (PSEN2) on chromosome 1 account for about 5–10 % of AD cases and are associated with early‑onset autosomal‑dominant disease[14]. The ε4 allele of apolipoprotein E (APOE) is the most important genetic risk factor for late‑onset AD; heterozygous carriers have a 3‑fold increased risk and homozygous carriers have a 15‑fold increased risk[15].

Other forms of dementia have distinct pathology. Vascular dementia results from ischemic or hemorrhagic cerebrovascular disease that causes stepwise cognitive decline[16]. Dementia with Lewy bodies is characterized by accumulation of α‑synuclein protein in cortical neurons and presents with fluctuating cognition, parkinsonism and visual hallucinations[17]. Frontotemporal dementia involves degeneration of the frontal and temporal lobes and manifests with personality changes, disinhibition and language difficulties[18]. Mixed pathology (e.g., AD with vascular contributions) is common[19].

Neuroinflammation and other mechanisms

Beyond plaques and tangles, neuroinflammation, oxidative stress and mitochondrial dysfunction play important roles. Microglial activation around Aβ plaques releases inflammatory mediators and reactive oxygen species that contribute to neuronal injury[20]. Dysregulation of metal homeostasis (iron, copper, zinc) and accumulation of toxic proteins such as TDP‑43 have also been implicated[21]. In Down syndrome (trisomy 21), an extra copy of APP leads to increased Aβ production; nearly all individuals with Down syndrome develop AD pathology by midlife[22].

Etiologic subtypes

The Diagnostic and Statistical Manual of Mental Disorders (DSM‑5) recognizes multiple etiological subtypes of major neurocognitive disorder: Alzheimer’s disease, vascular disease, frontotemporal lobar degeneration, Lewy body disease, Parkinson disease dementia, HIV infection, Huntington disease, prion disease, substance use, traumatic brain injury and others[23]. Multiple etiologies can coexist (e.g., mixed AD and vascular dementia), emphasizing the need for comprehensive evaluation.

Risk Factors and Epidemiology

Age is the strongest risk factor for dementia; prevalence doubles every five years after age 65[5]. Cardiovascular disease (CVD) is an important modifiable risk factor; it increases the risk of AD and vascular dementia[24]. Other modifiable factors include obesity and diabetes, which impair glucose tolerance and promote insulin resistance and chronic inflammation that accelerates Aβ accumulation[25]. Traumatic brain injury, depression, smoking, low educational attainment and hyperhomocysteinemia also contribute to risk[26]. Protective factors include higher education, estrogen use in women, anti‑inflammatory agents, cognitive leisure activities, a healthy diet and regular aerobic exercise[27].

The WHO lists additional modifiable risk factors: hypertension, high blood sugar, obesity, smoking, excessive alcohol consumption, physical inactivity, social isolation and depression[10]. A CDC analysis of adults aged ≥45 years identified eight modifiable risk factors hypertension, physical inactivity, obesity, diabetes, depression, current smoking, hearing loss and binge drinking and found that prevalence of subjective cognitive decline increased from 3.9 % among adults with no risk factors to 25 % among those with four or more[28]. Family history and genetic susceptibility, particularly the APOE ε4 allele, increase risk[15], while a first‑degree relative with AD raises the risk by 10–30 % and having two affected siblings triples the risk[26].

Global prevalence of dementia rose from 20.3 million in 1990 to 43.8 million in 2016[29]. Forecasts suggest that the number will reach 150 million by 2050[29]. Dementia currently affects over 55 million people worldwide[2], with more than 60 % living in low‑ and middle‑income countries[2]. Every 3.2 seconds someone develops dementia[30]. Women bear a disproportionate burden, experiencing higher disability‑adjusted life years and providing 70 % of informal care hours[31]. The global cost of dementia exceeded US$ 1.3 trillion in 2019 and is projected to rise to US$ 2.8 trillion by 2030[3][32].

Clinical Presentation and Staging

Dementia develops insidiously and progresses over years. Early symptoms include forgetting recent events, misplacing objects, getting lost in familiar environments, losing track of time and difficulty following conversations[33]. Personality and behavioral changes such as anxiety, agitation, apathy or inappropriate behaviours may precede cognitive symptoms[34]. As the disease advances, individuals may struggle with complex tasks, lose the ability to recognize loved ones, require assistance with activities of daily living and eventually become bedridden[35]. Neurologic symptoms vary by subtype Lewy body dementia presents with visual hallucinations, parkinsonism and REM sleep behaviours disorder[17]; frontotemporal dementia causes disinhibition and language impairment[18]; vascular dementia causes stepwise declines[16].

Staging systems

The Global Deterioration Scale (also called the Functional Assessment Staging – FAST) divides dementia into seven stages[36]:

No cognitive decline: Normal function; occasional memory lapses not apparent to others.
Very mild cognitive decline: Self‑perceived memory lapses but preserved function.
Mild cognitive decline: Increased memory lapses and occasional difficulty with work and social functioning; family notices subtle deficits.
Moderate cognitive decline: Clear difficulty in finances, planning and complex tasks; orientation problems; requires assistance with instrumental activities of daily living.
Moderately severe decline: Needs help with choosing clothing; may forget addresses and recent events.
Severe decline: Requires assistance with dressing, eating and toileting; personality changes; incontinence; agitation and wandering[37].
Very severe decline: Loss of verbal ability and psychomotor skills; requires total assistance; median survival 1.3 years in stage 7[38].

Early‑onset AD (before 65 years) represents about 5 % of cases and often follows a more aggressive course[39]. Late‑onset AD (after 65 years) is far more prevalent. Symptoms may plateau temporarily but overall progression is inevitable.

Diagnosis and Assessment

History and physical examination

Comprehensive history from the patient and caregivers is essential. Patients may present with memory loss, mood changes, social withdrawal, aggression, difficulty performing tasks and other cognitive deficits[40]. History should include comorbid conditions, medications and substance use. Clinicians must evaluate safety concerns such as driving, wandering, ability to use the telephone and vulnerability to abuse[41]. Family members often recognize deficits earlier than patients[42].

A focused physical and neurological examination assesses gait, reflexes and focal deficits. Differential diagnosis should consider depression (“pseudo‑dementia”), delirium, vitamin deficiencies, thyroid disorders and other reversible causes. Ataxia, visual changes, myoclonus or parkinsonism may suggest Creutzfeldt‑Jakob disease, Lewy body dementia or other atypical etiologies[17].

Cognitive screening tools

Multiple tools are available to quantify cognitive impairment. The Mini‑Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) are commonly used; the MoCA is more sensitive for mild cognitive impairment and takes about 10 minutes to administer[43]. The Mini‑Cog is a brief three‑minute screening tool; the Rowland Universal Dementia Assessment Scale (RUDAS) assists cross‑cultural assessment[44]. Scores provide a baseline and can monitor progression; they do not alone diagnose dementia because functional decline must also be present[45]. Nurses should perform periodic cognitive assessments and report changes[46].

Laboratory and imaging evaluation

Baseline laboratory tests include complete blood count, metabolic panel, vitamin B12, folic acid, thyroid function tests and syphilis and HIV serology[47]. Additional tests (erythrocyte sedimentation rate, heavy metal screen, Lyme disease titers, ceruloplasmin) may be indicated based on clinical suspicion[48]. Neuroimaging is important when the onset is early, progression is rapid, or diagnosis is uncertain. Magnetic resonance imaging (MRI) without contrast is typically the first study; computed tomography (CT) is used when MRI is contraindicated[49]. Positron emission tomography (PET) scans using amyloid or tau tracers assist in research and in selected clinical cases[50]. Cerebrospinal fluid analysis of Aβ and phospho‑tau provides additional biomarkers.

Diagnostic criteria and differential diagnosis

Definitive diagnosis of AD can only be made at autopsy; diagnosis in life is based on clinical criteria supported by biomarkers. The DSM‑5 criteria for major neurocognitive disorder require evidence of significant cognitive decline in one or more domains that interferes with independence in daily activities and does not occur exclusively in the context of delirium or mental disorders[19]. Clinicians must distinguish dementia from mild cognitive impairment, delirium, depression and normal ageing. Vascular lesions on imaging or a history of strokes suggest vascular dementia; fluctuating cognition and visual hallucinations suggest Lewy body dementia; early behavioral changes indicate frontotemporal dementia[17].

Management

Pharmacologic therapies

Management of dementia is largely symptomatic because there is no cure. Two main classes of drugs are approved for AD: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and the NMDA receptor antagonist memantine[51].

Donepezil is the medication of choice for mild dementia; it is a reversible inhibitor of acetylcholinesterase taken once daily[52]. Common adverse effects include gastrointestinal upset, bradycardia and syncope[53].
Rivastigmine is used in mild dementia and is available in oral and transdermal formulations; it inhibits both acetylcholinesterase and butyryl cholinesterase[54].
Galantamine is approved for mild dementia and is available in twice‑daily tablets or once‑daily extended release. It should be avoided in severe renal or hepatic dysfunction[55].
Memantine blocks NMDA receptors, reducing calcium influx and neuronal excitotoxicity. It is approved for moderate to severe AD and can be combined with cholinesterase inhibitors[56]. Side effects include dizziness, headaches and constipation[57].

Patients should be monitored for therapeutic response and adverse effects, and therapy should be discontinued if no meaningful benefit is observed or if side effects are intolerable[58]. New disease‑modifying therapies targeting amyloid clearance (aducanumab, lecanemab, donanemab) have received accelerated approval; they reduce amyloid burden and slow cognitive decline modestly but carry risks of amyloid‑related imaging abnormalities (ARIA)[59]. Clinicians must weigh benefits against risks and consider patient preference and cost.

Non‑pharmacologic and supportive interventions

Non‑pharmacologic strategies are fundamental. Regular physical exercise has been shown to slow progression of AD[60]. A healthy diet rich in fruits, vegetables, whole grains and lean proteins and low in processed foods may reduce risk and support brain health[61]. Cognitive stimulation through reading, puzzles, social engagement or learning new skills may build cognitive reserve. Sleep hygiene, exposure to sunlight and establishing a bedtime routine help improve sleep and reduce behavioral disturbances[62]. Creating a familiar and safe environment, providing security objects, redirecting attention, removing hazards and avoiding confrontational situations can minimize agitation and wandering[63]. Caregivers should join support groups and access community resources for education and respite[64].

Management of behavioral and psychological symptoms requires careful assessment. Anxiety and depression may be treated with selective serotonin reuptake inhibitors such as citalopram[65]. Antipsychotics may be necessary for severe agitation or psychosis but should be used at the lowest effective dose and for short durations due to increased risk of stroke and mortality[66]. Benzodiazepines should be avoided because they worsen delirium and increase falls[67].

Management of other dementias

Vascular dementia management focuses on controlling vascular risk factors hypertension, diabetes, hyperlipidemia, smoking cessation and exercise and using antiplatelet or anticoagulant therapy when indicated. Management of dementia with Lewy bodies includes cautious use of cholinesterase inhibitors for cognition and rivastigmine transdermal patches to reduce hallucinations; levodopa may improve motor symptoms but may worsen psychosis. Frontotemporal dementia lacks effective pharmacologic treatments; behavior modification, environmental adjustments and caregiver education are mainstays.

Nursing Management

Nurses play a central role in caring for patients with dementia throughout the disease trajectory. Their responsibilities include assessment, monitoring, education, coordination of care and support for patients and caregivers.

Assessment and monitoring

Nursing management focuses on promoting safety and enhancing quality of life[68]. Nurses should screen all older patients for early symptoms of cognitive decline and perform comprehensive assessments of cognition, mood, pain, functional status and safety[69]. Regular cognitive testing using tools such as the MMSE or MoCA establishes baselines and identifies progression[46]. Nurses must also assess for pain, anxiety, depression, delirium and medical conditions that patients may be unable to report verbally[69].

Safety and risk management

Nurses evaluate risks related to wandering, driving, medication adherence, falls and abuse[41]. Interventions include removing tripping hazards, installing locks or alarms, labelling rooms, supervising medication administration and assessing the need for assistive devices. Strategies such as night‑lights, reality orientation cues (clocks, calendars), memory aids and routine schedules can reduce confusion.

Education and support

Education is vital for patients and caregivers. Nurses teach about the disease process, symptom management, medication adherence, nutrition, exercise, sleep hygiene and stress reduction[70]. They encourage families to join support groups and provide information on respite services, adult day programmes and social resources[64]. Education about advance directives, power of attorney and end‑of‑life planning should occur early while decision‑making capacity remains[71].

Coordination of care and interprofessional collaboration

Care coordination reduces hospitalizations and emergency department visits[72]. Nurses liaise with physicians, social workers, occupational therapists, physical therapists, speech therapists and community agencies to tailor care plans. They facilitate transitions between home, hospital and long‑term care facilities and ensure continuity of information during handovers[73].

Discharge planning

Prior to discharge, the health‑care team must assess long‑term care needs and provide referrals for home services, rehabilitation or placement[74]. Discharge plans should include an updated medication list, allergy list, copies of legal documents (living will, advance directives, power of attorney, do‑not‑resuscitate orders) and scheduled follow‑up appointments[74]. Education should reinforce signs of dehydration, infection, agitation or other complications requiring immediate medical attention[75].

Palliative Care Considerations

Palliative care focuses on quality of life and can be integrated at any stage of dementia. In advanced stages, the median survival is about 1.3 years[38], yet many patients spend 40 % of their time in stage 7, often in skilled nursing facilities[76]. Prognostic tools such as the Advanced Dementia Prognostic Tool (ADEPT) and the Functional Assessment Staging (FAST) scale help estimate survival; hospice eligibility in the United States usually requires FAST stage 7 and at least one medical complication (aspiration pneumonia, sepsis, multiple pressure ulcers, recurrent fevers or weight loss)[77].

The American Academy of Family Physicians advises that palliative care be considered early—sometimes as early as stage 2—and that it can coexist with curative treatment[78]. Palliative services include symptom management, goals‑of‑care discussions, code status decisions and psychosocial support[79]. Advance care planning should occur while cognitive function allows; discussions should clarify patient preferences, designate surrogate decision makers and address resuscitation and life‑sustaining treatment[80]. Educational resources such as the Institute for Healthcare Improvement’s Conversation Starter Kit and dementia‑specific advance directives can guide these conversations[80].

Pain is prevalent in advanced dementia, occurring in up to 50 % of palliative care patients[81]. Because patients may be unable to verbalize discomfort, nurses should use validated tools such as the Pain Assessment in Advanced Dementia (PAINAD) scale, which evaluates breathing, vocalization, facial expression, body language and consolability[82]. Agitation and dyspnea may be manifestations of pain or unmet needs[83]. Treating pain should be targeted to the type (nociceptive vs neuropathic) and severity; opioids may be necessary, but non‑pharmacologic strategies (massage, repositioning) should also be employed.

Other recommendations for advanced dementia include: educating caregivers about the progressive and ultimately fatal nature of the disease, initiating advance care planning early, ensuring that advance directives are in place, offering palliative care alongside other medical care by stage 5 or 6, managing neuropsychiatric, pain, incontinence and sleep symptoms appropriately, recommending caregiver support to prevent burnout and considering hospice evaluation at stage 7[84]. Nurses can counsel families that palliative care is supportive of ongoing treatment and that other comorbidities will continue to be treated[85].

Case Presentation

Patient history and presentation

Patient: Mrs. J., a 77‑year‑old widow and retired schoolteacher, lives with her daughter. She has a history of hypertension, type 2 diabetes mellitus, hyperlipidemia and depression. There is no family history of dementia. She completed high school but had no further formal education.

Presenting complaints: Over the past two years Mrs. J. has exhibited progressive forgetfulness. She misplaces objects, repeats questions, forgets recent conversations and becomes lost when driving to familiar places. Her daughter reports mood swings, irritability and withdrawal from social activities. She mismanages her finances and medications. She had two minor falls in the past six months and has lost 4.5 kg unintentionally.

Risk factors: Advanced age (77 years), hypertension and diabetes (vascular risk factors), obesity in mid‑life, depression and social isolation are recognized modifiable risk factors for dementia[86][10]. On physical examination, her blood pressure is 150/88 mm Hg, body mass index is 26.5 kg/m² and she is physically inactive. She does not smoke or drink alcohol.

Assessment findings

Cognitive assessment: The Mini‑Mental State Examination (MMSE) score is 21/30 (moderate impairment). Deficits are noted in short‑term memory, attention and executive function. The Montreal Cognitive Assessment (MoCA) score is 19/30, consistent with mild cognitive impairment/early dementia[44]. Repetition of tests after three months shows a decline of three points on the MMSE.

Functional assessment: She requires reminders for medication administration and help balancing her chequebook. She can perform personal care but needs assistance with meal planning and grocery shopping (instrumental activities of daily living). The Functional Assessment Staging (FAST) places her at stage 4.

Physical examination: She appears well nourished. Neurological examination reveals slightly slowed gait but no focal deficits. There is no tremor or parkinsonism. Mood is depressed but she denies suicidal ideation. She reports poor sleep and decreased interest in hobbies.

Laboratory tests: Complete blood count, metabolic panel, thyroid‑stimulating hormone, vitamin B12 and folate are normal. HbA1c is 7.8 %. Serum cholesterol is elevated. MRI of the brain shows mild cerebral atrophy and scattered white matter hyperintensities suggestive of small vessel ischemic changes.

Diagnosis

Based on progressive cognitive decline interfering with instrumental activities of daily living, absence of delirium and exclusion of reversible causes, Mrs. J. is diagnosed with probable Alzheimer’s disease with vascular contributions. Her cardiovascular comorbidities and MRI findings support mixed AD and vascular dementia[87].

Nursing diagnoses

Disturbed thought processes related to progressive neurodegeneration as evidenced by memory loss, disorientation and impaired problem solving.
Risk for injury related to cognitive impairment, impaired judgment and history of falls.
Impaired memory related to Alzheimer’s disease as evidenced by forgetting recent events and misplacing objects.
Caregiver role strain related to increasing care demands, emotional stress and insufficient support.
Deficient knowledge related to disease process and management.

Plan of care and interventions

The overarching goals are to maintain Mrs. J.’s safety and quality of life, slow functional decline, manage comorbidities, support her daughter and plan for future care.

Pharmacologic management

Initiate donepezil 5 mg nightly and titrate to 10 mg after four weeks if tolerated to enhance cholinergic transmission[52].
Discuss potential side effects (nausea, diarrhoea, bradycardia); monitor heart rate and blood pressure[53].
Continue antihypertensive therapy and statin for vascular risk reduction. Emphasize strict glycaemic control and monitor HbA1c.
Evaluate the need for memantine if cognitive decline progresses to moderate stage[56].
Avoid anticholinergic medications and benzodiazepines to reduce cognitive adverse effects and falls[67].

Non‑pharmacologic interventions

Develop a structured daily routine with scheduled activities, meals and rest to reduce confusion. Use calendars, clocks and labelled cupboards for orientation.
Encourage physical activity such as walking 20–30 minutes daily and chair exercises to improve cardiovascular health and slow cognitive decline[60].
Recommend a Mediterranean‑style diet rich in fruits, vegetables, legumes, whole grains, fish and unsaturated fats and low in processed foods[61].
Introduce cognitive stimulation (crossword puzzles, reminiscence therapy, music therapy) to maintain cognitive reserve.
Establish good sleep hygiene by limiting daytime naps, creating a restful environment, increasing daytime sunlight exposure and maintaining a consistent bedtime[62].
Provide strategies to reduce agitation (e.g., reduce noise, avoid confrontational situations, distract with meaningful tasks)[63].

Safety interventions

Remove tripping hazards (rugs, clutter) and install grab bars and night‑lights.
Assess driving ability; recommend discontinuation if safety is compromised and arrange alternative transportation.
Use medication pill organizers or blister packs; involve daughter in medication administration.
Provide an identification bracelet with name, address and contact number and consider a GPS‑enabled device in case of wandering.
Assess home for fire safety; ensure working smoke detectors and that she does not use the stove unsupervised.

Education and caregiver support

Explain the disease process, prognosis and available treatments to Mrs. J. and her daughter in simple, empathetic terms. Clarify that cholinesterase inhibitors slow symptom progression but do not cure the disease[51].
Discuss modifiable risk factors and encourage lifestyle changes to control hypertension, diabetes and hyperlipidemia[86].
Provide information on local Alzheimer’s Association resources, respite services, adult day programmes and caregiver support groups[64].
Encourage the daughter to attend counselling to manage stress and to seek help from other family members. Highlight the importance of regular breaks to prevent caregiver burnout[84].

Advance care planning and palliative care

Initiate discussions about advance directives and designate a durable power of attorney for health care. Encourage documentation of preferences for life‑sustaining treatments while Mrs. J.’s decision‑making capacity remains[80].
Introduce the concept of palliative care as supportive care that can be integrated early; emphasize that it focuses on quality of life and is provided alongside disease‑directed treatments[79].
Plan for potential transitions to assisted living or nursing home when safety at home becomes compromised. Provide information on hospice services when FAST stage 7 criteria are met[84].
Educate on recognizing pain and using tools such as the PAINAD scale for non‑verbal pain assessment[83]. Offer non‑pharmacologic pain management strategies and discuss opioid use if necessary.

Implementation and outcomes

Mrs. J. and her daughter agree to start donepezil. After six weeks her MMSE score stabilizes at 21 and she reports fewer episodes of confusion. Mild gastrointestinal side effects resolve after two weeks. The daughter attends a caregiver support group and expresses feeling less overwhelmed. She implements medication reminders and safety modifications. Mrs. J. begins walking with a friend, engages in knitting and enjoys music therapy. An advance directive is completed naming her daughter as surrogate decision maker. Palliative care is introduced during a family meeting; the team discusses goals of care and emphasises comfort and dignity.

Evaluation

Regular follow‑up visits every three months will evaluate cognitive function, functional status, behavioral symptoms, adherence to interventions and caregiver burden. The nurse will monitor blood pressure, heart rate and weight at each visit. Progression to a higher FAST stage or increased falls will trigger re‑evaluation of driving and living arrangements. The care plan will be adjusted as the disease advances, incorporating palliative care and considering memantine or hospice when appropriate.

Discussion

Mrs. J.’s case illustrates typical features of early Alzheimer’s disease with vascular contributions. Her risk factors advanced age, hypertension, diabetes, mid‑life obesity and depression are consistent with epidemiologic data linking vascular and metabolic factors to dementia[86][10]. Mixed pathology is common; white matter hyperintensities on MRI suggest cerebrovascular disease. Early recognition allowed initiation of donepezil, which may provide modest cognitive benefits[52]. More so non‑pharmacologic strategies such as exercise, diet and cognitive stimulation are crucial and may slow progression[62].

The case underscores the nurse’s role in assessment, care planning, education and support. Nurses monitor cognitive and functional status, identify safety issues and coordinate services[68][72]. They educate patients and caregivers about symptom management and disease expectations[70]. Importantly, they facilitate advance care planning and refer to palliative care early[71]. Nurses must recognise caregiver burden and provide resources for support[84].

The palliative care guidelines emphasize that care should be aligned with patient goals and introduced early rather than reserved for the final months[79]. Prognostic tools such as ADEPT and FAST can aid in hospice eligibility determinations[77]. Pain management in non‑verbal patients requires validated assessment tools like PAINAD[88]. Education about the terminal nature of dementia and the benefits of advance directives helps families prepare for end‑of‑life decisions[84]. The emphasis on caregiver support acknowledges the intense demands of caring for a person with dementia[31].

Conclusion

Dementia represents a growing global public health challenge with profound social and economic consequences. Therefore, Alzheimer’s disease is the leading cause, but mixed pathologies are common. Pathogenesis involves amyloid‑β plaques, neurofibrillary tangles, neuroinflammation and other mechanisms. More so, age and genetics are major determinants, yet many cases could potentially be delayed or prevented by addressing modifiable risk factors such as hypertension, diabetes, obesity, depression, smoking, physical inactivity and social isolation[86][10]. Early diagnosis through history, cognitive testing, laboratory evaluation and neuroimaging enables timely interventions and planning. Management is primarily symptomatic; cholinesterase inhibitors and memantine provide modest benefits and emerging disease‑modifying therapies offer hope for slowing progression[51][89]. Non‑pharmacologic strategies, caregiver education and support are essential components.

Nurses play a pivotal role across the continuum from screening and assessment to care coordination, patient and family education, and advocacy for palliative care. They must assess and manage symptoms, ensure safety, support caregivers and facilitate advance care planning and transitions. Integrating palliative care early improves quality of life and aligns interventions with patient values. As the global burden of dementia rises, comprehensive, patient‑centered care grounded in evidence‑based practice and interprofessional collaboration will be essential to support individuals like Mrs. J. and their families.

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