Dementia: the neurocognitive disorders

• Dementia is no longer an official diagnosis in the DSM-5-TR framework: it is major neurocognitive disorder, a recognisable clinical syndrome of significant decline in cognition that interferes with independence, with mild neurocognitive disorder as its earlier, self-managing stage.
• Most dementia is permanent and progressive; Alzheimer disease accounts for 60–70% of cases and vascular change is the next most common.
• Diagnosis is clinical: history from the person and someone who knows them, examination, cognitive testing interpreted for age and education, and exclusion of reversible causes.
• Management is not a single drug: carer support, cognitive stimulation, environmental measures, treatment of mood and pain, and cholinesterase inhibitors or memantine for suitable subtypes.
• Safety work (capacity, driving, safeguarding, fall prevention) often matters more than the prescription. Non-drug measures come first for distress.

By the end of this page you should be able to:

1. Define major and mild neurocognitive disorder in DSM-5-TR terms and separate them from delirium and normal ageing.
2. List the common causes of dementia and distinguish the main subtypes by their clinical picture.
3. Choose and interpret screening cognitive tests, including their usual cut-offs.
4. Separate depression with cognitive symptoms ("pseudodementia") from dementia using bedside clues.
5. Plan management of cognition, behaviour and mood, including when and how to use antipsychotics.
6. Carry out, or at least initiate, capacity and safety assessments and know when and to whom to refer.

A neurocognitive disorder is a decline from a previously attained level of cognitive function. Dementia in everyday practice is the syndrome called major neurocognitive disorder: a substantial decline in one or more of the DSM-5-TR cognitive domains, sufficient to interfere with independence in everyday activities, not occurring exclusively during delirium and not better explained by another mental disorder. The domains are complex attention, executive function, learning and memory, language, perceptual-motor (visuospatial) function, and social cognition. ^[2] Mild neurocognitive disorder corresponds to mild cognitive impairment: a modest decline in one or more of the same domains, with independence preserved but greater effort, accommodation or compensatory strategies needed. ^[2]

The syndrome is deliberately named without tying it to age or to Alzheimer disease, because younger people can be affected and the cause can be vascular, Lewy body, frontotemporal, traumatic, infective or metabolic. ^[2]

Delirium differs in three ways: onset over hours to days, marked fluctuation, and a core deficit in attention and awareness rather than in memory alone. It is the thing to rule out before calling a cognitive decline dementia. ^[2]

Etiological subtypes are specified as "due to" one of: Alzheimer disease; cerebrovascular disease; frontotemporal lobar degeneration; Lewy body disease; Parkinson disease; traumatic brain injury; HIV infection; Huntington disease; prion disease; another medical condition (for example HIV or hypothyroidism); multiple etiologies; or unspecified. Each can be qualified as probable or possible, depending on the certainty of the cause. ^[2]

Major versus mild is not a two-step staging of one disease so much as a functional line. A person can live alone with mild neurocognitive disorder for years; the move to major is marked by loss of the ability to manage finances, medications, meals, transport or personal care. ^[2]

Worldwide, about 57 million people were living with dementia in 2021, over 60% of them in low- and middle-income countries, with nearly 10 million new cases each year. ^[1] Women are disproportionately affected, because of longer life expectancy and because women provide around 70% of care hours. ^[1]

In high-income countries prevalence is roughly 5–10% of people aged 65 years and over and rises exponentially with age, doubling about every five years after 65. ^[2] The annual incidence increases from about 0.1% in those aged 60–64 to about 8.6% in those aged 95. ^[2] Alzheimer disease is the most common form, contributing to 60–70% of cases. ^[1][2] Dementia is the fifth leading cause of death globally and one of the leading causes of disability and dependency in older people. ^[1]

Up to 9% of all cases are young-onset, with symptoms beginning before 65 years. ^[1] Prevalence is lower in sub-Saharan Africa and higher in Latin America than in other world regions, and is elevated in Black and Latino groups in the United States. ^[2] A review published in the 2010s estimated 35.6 million people worldwide with dementia in 2010 and 115.4 million by 2050; the numbers continue to rise with population ageing. ^[2]

Dementia cost the global economy about US$ 1.3 trillion in 2019, of which about half was informal carer time at roughly 5 hours of care and supervision a day. ^[1]

The commonest cause is Alzheimer disease. ^[1] The DSM-5-TR recognises the major causes as vascular (the second most common); dementia with Lewy bodies and Parkinson disease dementia; frontotemporal lobar degeneration; prion disease; traumatic brain injury; substance or medication use; another medical condition; and mixed or multiple etiologies. ^[2] Less common causes include Huntington disease, normal pressure hydrocephalus, chronic subdural haematoma, brain tumour, HIV-associated neurocognitive disorder, vitamin B12 or thiamine deficiency, hypothyroidism, syphilis and alcohol-related brain injury. ^[2] Boundaries between types are blurred and mixed dementia is common. ^[1]

Always exclude treatable or partly reversible causes before settling on a neurodegenerative diagnosis: delirium, depression, medication with high anticholinergic burden, sensory impairment, metabolic or vascular insults, infection, and structural lesions. ^[3][2]

Age is the dominant risk factor. Beyond age, the evidence supports attention to midlife vascular risk: hypertension, diabetes, high body mass index, high cholesterol, heart failure, atrial fibrillation and stroke all increase risk. ^[2] Lower educational attainment, low socioeconomic position, smoking, harmful alcohol use, physical inactivity, social isolation, depression, head injury, obstructive sleep apnoea and air pollution are also risk factors; many act decades before symptoms. ^[1][2]

Genetics matter in two different ways. Deterministic mutations cause rare early-onset disease (amyloid precursor protein, presenilin 1 and 2 in Alzheimer disease; Notch 3 in CADASIL; Huntington trinucleotide repeat; APP and tau mutations in some frontotemporal dementias). Susceptibility alleles such as APOE*4 raise risk but are neither necessary nor sufficient for diagnosis and are not a diagnostic test. ^[2]

Protective factors point to brain and cognitive reserve: higher education, bilingualism, cognitively and socially engaging work and leisure, physical activity, Mediterranean-style diet and management of vascular risk. Reverse causality is hard to exclude, because brain pathology may begin decades before symptoms. ^[2][1]

Whatever the cause, the dementia syndrome emerges when brain pathology has accumulated past the brain's ability to compensate. The route from molecule to symptom is different for each subtype.

• Alzheimer disease. Amyloid plaques and neurofibrillary (tau) tangles build up, synapses and then neurons die, and cholinergic transmission is reduced. Early damage is in medial temporal memory circuits, so new learning and recent memory fail first; executive, language and visuospatial functions follow later. ^[2]
• Vascular. Large or small vessel disease injures white matter and strategically placed grey matter; lesions anywhere disrupting frontal-subcortical circuits produce executive, attention and gait deficits, often stepwise or fluctuating, and often combined with depressive symptoms. ^[2]
• Lewy body dementia. Alpha-synuclein accumulates in Lewy bodies; cholinergic and dopaminergic pathways are affected, leading to fluctuating alertness, visual hallucinations and parkinsonism, with attention and visuospatial failure earlier than memory failure. ^[2]
• Frontotemporal lobar degeneration. Focal atrophy of frontal and temporal lobes (tau or TDP-43 pathology) changes behaviour, personality, language or empathy, often before memory is obviously impaired. ^[2]

Why symptoms appear later than pathology: brain reserve means people tolerate silent damage for years; once compensatory networks are exhausted, decline becomes visible. This is why vascular and lifestyle risk act decades before diagnosis. ^[2]

Behavioural and psychological symptoms (BPSD) arise because neurodegeneration hits the circuits for emotion, motivation, perception and executive control, not just memory. Apathy, depression, anxiety, irritability, hallucinations, delusions, wandering, agitation and sleep or eating disturbances are the syndrome's most distressing features for families. ^[5]

Dementia usually begins insidiously and progresses; neither the person nor the family notices a single event. Memory difficulty tends to be the presenting complaint ("losing things, repeating questions"), but ask about function, not memory alone: managing money, medicines, cooking, transport, hobbies and social engagements. ^[2]

Use the DSM-5-TR cognitive domains as a checklist of what daily tasks test each one: ^[2]

A reliable informant is usually the best historian, but in very early disease the person may be more aware than the family. ^[2] Clues to declining cognition include missed appointments, forgotten prescriptions, vague or evasive answers, catastrophising of tiny problems, and reports of mood or behavioural change before any "memory" complaint. ^[2]

Ask about agitation, hallucinations, delusions, depression, anxiety, apathy, disinhibition, wandering, disturbed sleep and altered appetite or eating. These are both diagnostic pointers (visual hallucinations suggest Lewy body dementia, florid disinhibition suggests frontotemporal) and the main targets for management. The Neuropsychiatric Inventory is the standard structured way to record them. ^[6]

Record general appearance, mood and engagement, and do a structured mental state examination: orientation, attention, short-term recall, autobiographical memory, naming, fluency, visuospatial construction (cube or clock drawing), executive tests (digit span reversed, verbal fluency, sequencing). ^[2] Screen mood with a simple tool such as the 15-item Geriatric Depression Scale. ^[7]

On physical examination look for stroke signs, vascular risk factors, parkinsonism (tremor, rigidity, bradykinesia), gait disorder, sensory impairment and cortical reflexes. ^[2][3] Gait, focal neurological signs and primitive reflexes help pick up less common causes. ^[2]

The first decision is whether the person has normal ageing, mild cognitive impairment, or dementia. The second is whether the cause is neurodegenerative or reversible. ^[2]

Pseudodementia is covered in more detail below; the key point is that the two can coexist. Mixed dementia and depression occurring together is common, especially vascular dementia, Parkinson disease dementia and Huntington disease dementia. ^[7]

Subtype clues: an insidious memory-first decline with preserved behaviour points to Alzheimer disease; stepwise decline with vascular risk to vascular dementia; fluctuating alertness, visual hallucinations and parkinsonism to dementia with Lewy bodies; early behavioural disinhibition and language loss with spared episodic memory to frontotemporal disease; cognitive decline after an established diagnosis of Parkinson disease to Parkinson disease dementia. ^[2][4] For the full subtype picture, see the MedGrasp topics "Alzheimer disease and the dementias: approach" and "Vascular, frontotemporal and Lewy body dementia" as plain text.

Take a history from the person and (where possible) someone who knows them well, perform a physical and neurological examination, and order appropriate blood and urine tests before settling on a neurodegenerative diagnosis. ^[3][2] A reasonable screen includes: full blood count, urea and electrolytes, liver function, calcium, glucose, thyroid function tests, vitamin B12 and folate, and syphilis/HIV testing where history or geography suggests it, plus review of all medicines for anticholinergic burden. ^[3][2]

Brief instruments are aids, not diagnoses. NICE NG97 recommends a validated brief structured cognitive instrument such as the 10-point cognitive screener, the 6-item cognitive impairment test, the 6-item screener, the Memory Impairment Screen, the Mini-Cog, or Test Your Memory. ^[3] Usual cut-offs and administration times come from the Alzheimer's Association validation work. ^[8]

Do not rule dementia out simply because a person scores normally on a cognitive instrument. ^[3]

Informant instruments such as the IQCODE, FAQ, AD8 and Quick Dementia Rating System add history about change from previous ability and are especially useful when the person has little insight. ^[8]

Neuropsychological testing is the gold standard for mild or atypical impairment; brief screens are usually sensitive enough for dementia but not for mild neurocognitive disorder. ^[2]

Brain imaging (CT or MRI) is used to exclude treatable causes and, with expert interpretation, to support a subtype diagnosis. ^[2] Nuclear medicine, lumbar puncture (CSF tau, amyloid) and amyloid PET are mainly specialist and research tools; NICE NG97 refers rapidly progressive suspected Creutzfeldt–Jakob disease to a neurological service. ^[3] SPECT and PET in selected cases help separate depression from neurodegeneration. ^[7]

Major neurocognitive disorder (dementia): significant cognitive decline in one or more domains, based on concern from the person, an informant or the clinician plus substantial impairment on objective testing; interference with independence in everyday activities; not exclusively during delirium; not better explained by another mental disorder. ^[2]

Mild neurocognitive disorder (MCI): modest cognitive decline in one or more domains, with the same concern and modest objective impairment; independence preserved, although tasks take longer or need compensation; decline from a previous level documented by history and objective assessment; not exclusively delirium and not better explained by another mental disorder. ^[2]

Then specify etiology ("due to Alzheimer disease", "due to cerebrovascular disease", and so on), and qualify each as probable or possible depending on the certainty of the evidence. ^[2]

Diagnostic, imaging and biomarker criteria from the National Institute on Aging–Alzheimer's Association are the companion frameworks for Alzheimer disease specifically, and are used alongside the DSM-5-TR descriptive syndromic diagnosis. ^[2]

Severity is usually staged clinically by interview, from very mild through mild, moderate and severe. The Clinical Dementia Rating and Functional Assessment Staging (FAST) systems describe overall severity and the sequence of functional loss from mild cognitive impairment to severe dementia. ^[8] These help with prognosis, care planning and eligibility (for example for services and support) rather than with diagnosis.

Pseudodementia is cognitive impairment mimicking dementia but arising from depression, not neurodegeneration. It is a clinical concept, not an official diagnosis. ^[7] In older adults with cognitive complaints, estimates suggest between 2% and 32% actually have pseudodementia. ^[7] The two conditions overlap heavily and frequently coexist; depression is itself a risk factor for later dementia and a recognised prodrome. ^[7]

Bedside differences (table excerpted from a 2023 narrative review): ^[7]

The 15-item Geriatric Depression Scale is useful here: scores above 5 are suggestive of depression and 10 or above almost always indicate depression. ^[7] Imaging tends to show atrophy and ventricular enlargement in dementia; functional depression usually does not. ^[7]

Diagnosing needs a careful history, exclusion of B12 deficiency, thyroid disease and vascular or infectious causes, neuropsychological testing when doubt remains, and, in selected cases, functional neuroimaging. ^[7]

Management runs in parallel: manage the person, the carer, the home, any reversible disease, the symptoms, and the behaviour.

• Provide information about the subtype, expected course, who is involved and how to contact them; correct myths. ^[3]
• Name a single coordinator of care. ^[3]
• Offer a care plan, reviewed and updated. ^[3]
• Give early and repeated opportunities for advance planning: lasting power of attorney, advance statements, advance decisions to refuse treatment, and preferred place of care and death. ^[3]
• Arrange access to a memory service or equivalent multidisciplinary service. ^[3]

• Group cognitive stimulation therapy for mild to moderate dementia. ^[3]
• Consider reminiscence therapy and cognitive rehabilitation or occupational therapy to maintain skills. ^[3]
• Tailored activities, meaningful routines, sensory aids (glasses, hearing aids), social engagement and physical activity. ^[1][3]
• Do not offer acupuncture, ginseng, vitamin E supplements or herbal formulations for dementia. ^[3]

Offer carers psychoeducation and skills training from diagnosis: education, personalised strategies, communication training, advice on maintaining their own physical, emotional and spiritual health, enjoyable shared activities and information on services. ^[3] Carer burnout is one of the main reasons people with dementia end up in institutional care; supporting the carer is a clinical intervention. ^[1]

No drug cures dementia. Choice depends on subtype and severity:

• Donepezil, galantamine and rivastigmine (acetylcholinesterase inhibitors) are recommended as monotherapy for mild to moderate Alzheimer disease, and as an option in dementia with Lewy bodies. ^[3][2]
  • Donepezil: start 5 mg once daily at bedtime; after 1 month reassess and increase to a maximum of 10 mg once daily if needed and tolerated. ^[4]
  • Galantamine: start 8 mg once daily for 4 weeks, then 16 mg once daily for at least 4 weeks; maintenance 16 to 24 mg once daily. ^[4]
  • Rivastigmine: start 1.5 mg twice daily; increase in 1.5 mg twice daily steps at intervals of at least 2 weeks to a maximum of 6 mg twice daily; or 4.6 mg patch daily, increased to 9.5 mg patch after at least 4 weeks. ^[4]
• Memantine: 5 mg once daily initially, increasing in 5 mg steps at weekly intervals to a maximum of 20 mg daily; licensed for moderate to severe Alzheimer disease. ^[4] It is well tolerated and may also be used when cholinesterase inhibitors are not tolerated. ^[2]
• Vascular disease and risk: strict control of blood pressure, lipids and glucose slows further vascular damage. ^[1]
• Cholinesterase inhibitors are not beneficial and may worsen behaviour in frontotemporal dementia; they are not evidence-based in other subtypes. ^[2]
• Mild cognitive impairment: there is minimal evidence of benefit and a real risk of gastrointestinal side effects, so routine use is not justified. ^[2]
• Benzodiazepines are usually avoided in dementia because of paradoxical agitation, falls and further cognitive decline. ^[2]

Always check local formularies, comorbidities (for example bradycardia for cholinesterase inhibitors, renal impairment for memantine), and monitor for nausea, weight loss and syncope.

Treat depression with psychotherapy and antidepressants; depression in dementia can usually be treated. ^[7] Selective serotonin reuptake inhibitors help severe depressive symptoms in people living with dementia if non-drug measures fail, but they should not be the first option. ^[1] Vortioxetine, an antidepressant with serotonergic activity, may improve cognitive symptoms of depression independent of mood effect. ^[7] Because depressive pseudodementia often improves with treatment, a trial of adequate antidepressant therapy is reasonable when depression is suspected. ^[7]

Assessment comes first: a structured assessment of the type, frequency, severity, pattern and timing of the behaviour, plus any modifiable contributor (pain, delirium, infection, constipation, thirst, sensory loss, inappropriate care, environment, over-sedation). ^[6]

• Offer psychosocial and environmental interventions as initial and ongoing management: reduce noise and clutter, keep routine, simplify tasks, reassure, use familiar music or activities, involve in meaningful tasks, support caregivers. ^[3][6]
• Detect and treat the physical cause before prescribing.
• Reassess regularly; symptoms fluctuate.

Antipsychotics only when the person is at risk of harming themselves or others, or is experiencing agitation, hallucinations or delusions causing severe distress. ^[3] The APA (2016) Practice Guideline sets out the standard principles, summarised here via a 2016 clinical update: ^[6]

• Try non-drug approaches first and document the response. ^[6]
• Review risks and benefits with the patient (if feasible) and the surrogate decision maker and family. ^[6]
• Start at a low dose and titrate up slowly to the minimum effective dose. ^[6]
• If there is no clinically significant response after a 4-week trial at an adequate dose, taper and withdraw. ^[6]
• In responders, attempt to taper and withdraw within 4 months of starting; assess at least monthly during the taper and for at least 4 months after stopping. ^[6]
• Avoid haloperidol as first-line in a non-emergency setting; avoid long-acting injectable antipsychotics unless a co-occurring chronic psychotic disorder needs them. ^[6]
• Second-generation antipsychotics are preferred when one is needed; use particular caution in Lewy body dementia. ^{[2] [5]}
• Note the regulatory warning about cerebrovascular risk and mortality in older people with dementia and the MHRA advice; antipsychotic use is off-label for almost all agents. ^[3]
• Haloperidol and risperidone are only considered with caution, under close supervision, when the person is at risk of harm to self or others. ^[1]

The decision to prescribe is one of the highest-stakes judgements in dementia care; revisit it monthly.

From diagnosis onwards offer flexible, needs-based palliative care rather than reserving it for the end. ^[3] Special attention is needed for eating and drinking difficulties (comfort feeding, mouth care), pain in people who cannot communicate (use validated observational scales), and infections, where antibiotics may or may not be appropriate. ^[3]

• Refer for specialist dementia diagnosis when cognitive and functional decline persist after reversible causes are investigated. ^[3]
• Suspected rapidly progressing dementia (possible Creutzfeldt–Jakob disease) to neurology with CSF examination. ^[3]
• Neuropsychology when it is unclear whether impairment is present, whether it is dementia, or which subtype. ^[3]
• Geriatric psychiatry for severe behavioural or psychiatric symptoms, complex capacity, or medication problems.
• Social work referral for carer breakdown, unsafe living conditions, or institutional care risk.

Capacity is decision-specific and time-specific. In UK practice this is governed by the Mental Capacity Act 2005. ^[3]

• Assess consent to share information, which people and what information, and document it at, and after, diagnosis. ^[3]
• Give special consideration to people without capacity, using best-interests decision-making. ^[3]
• Plan ahead early, while capacity exists: lasting power of attorney for health/welfare and property/finance; advance statements; advance decisions to refuse treatment; preferences for place of care and death. Review these at every care review. ^[3]
• Capacity for driving must be assessed and the person must notify the relevant licensing authority and insurer; this is an urgent, high-risk area. ^[3]
• Safeguard against abuse and exploitation, falls, medication errors, wandering and self-neglect; include home hazards, fire risk and wandering, and review the medicines list.
• Carers need breaks, training and respite; carer breakdown is common and preventable. ^[3]

Law on capacity, driving and consent differs between countries; the principles (support the person, assess decision by decision, plan early) are widely transferable.

• Young-onset dementia (under 65) accounts for up to 9% of cases. ^[1] It affects work, parenting, driving and finance, and usually signals less typical causes or genetic disease; refer to specialist assessment. ^[2]
• Children and adolescents: true dementia is rare and should trigger a search for reversible, metabolic, genetic or infective causes rather than normal neurodegeneration. ^[2]
• Older adults: balance benefits against harm. Reduce anticholinergic burden, treat falls risk factors, review medicines that worsen cognition, and treat depression and pain. Cholinesterase inhibitors need monitoring for bradycardia and gastrointestinal side effects. ^[2][4]
• Pregnancy: dementia is rare, but women are the majority of carers. Many dementia drugs lack robust pregnancy safety data; any treatment in pregnancy or lactation should be decided with obstetric and psychiatric specialists. ^[1]
• Immunocompromised (for example HIV): HIV-associated neurocognitive disorder is usually partly reversible with effective antiretroviral treatment; always screen for reversible causes. ^[2]
• People with delirium-prone frailty: minimise hospital disruption, constipation, dehydration and urinary retention. ^[2]

There is no cure yet; the realistic ambition is risk reduction and early detection. ^[1] Evidence supports risk reduction across the life course: ^[1]

• be physically active;
• do not smoke;
• avoid harmful alcohol use;
• eat a healthy, balanced diet;
• stay socially and cognitively active;
• maintain a healthy weight;
• manage blood pressure, cholesterol and blood sugar;
• use hearing aids when needed;
• reduce exposure to air pollution.

Midlife vascular and educational factors dominate; social determinants such as poverty, limited education and unequal access to employment and health care matter too. ^[1][2]

Screening. The guidelines used here do not recommend routine screening of asymptomatic people. ^[8] Assessment is triggered by concern from the individual, family, carer or clinician, or by repeated missed appointments, medication errors and quiet withdrawal. Reversible causes are then excluded. Early recognition still matters: it allows support, safety planning, carer preparation and access to evidence-based treatments, and it preserves the person's legal autonomy for as long as possible. ^[3][1]

• Functional decline across all activities of daily living; eventual total dependence. ^[2]
• Falls, fractures, wandering, traffic and home accidents.
• Infections (respiratory, urinary), dehydration, malnutrition and pressure ulcers.
• Aspiration, swallowing difficulties and weight loss.
• Behavioural emergencies: severe agitation, aggression, hallucinations and distress.
• Carer strain, depression and burnout; the carer often becomes the "second patient". ^[1]
• Polypharmacy, sedative harm and anticholinergic side effects.
• Institutionalisation and, in advanced dementia, inability to communicate and loss of dignity if not actively prevented.
• Mortality: dementia is the fifth leading cause of death globally. ^[1]

Dementia is progressive. In Alzheimer disease the average survival after the onset of dementia is about 10 years, but varies widely with age of onset, severity, comorbidity and other factors. ^[2] Lewy body and vascular forms often have shorter courses and higher risk of functional loss from falls and stroke; frontotemporal disease can run more quickly once advanced. ^{[2][4] [7]}

Prognosis is not a number for one person. Decline is often punctuated by vascular events and intercurrent illness. Many people with dementia die of intercurrent causes; recognition early allows advance care planning that keeps the final illness aligned with the person's wishes. ^[3]

Importantly, a person can have a good quality of life for years with support: cognitive stimulation, meaningful relationships, freedom from pain and fear, and respect for identity matter more than any single drug. ^[3]

The following MedGrasp topics, by plain name, cover the subtypes and related areas: Alzheimer disease and the dementias: approach; Vascular, frontotemporal and Lewy body dementia; and the common geriatric syndromes that complicate dementia care.

• Dementia is major neurocognitive disorder: significant cognitive decline in one or more DSM-5-TR domains, interfering with independence, not delirium, not another mental disorder.
• Mild neurocognitive disorder (MCI) is the earlier stage with preserved independence but extra effort.
• Alzheimer disease contributes 60–70% of cases; vascular disease is the next most common and mixed aetiology is frequent. ^[1]
• About 57 million people worldwide lived with dementia in 2021; nearly 10 million new cases occur each year.
• Diagnosis is clinical: history from person and informant, examination, interpreted cognitive testing, and exclusion of reversible causes.
• Pseudodementia (depression presenting as cognitive decline) is reversible and potentially treatable; the two coexist often.
• Cholinesterase inhibitors (donepezil 5 to 10 mg, galantamine 8 to 24 mg, rivastigmine 1.5 to 6 mg twice daily, or patches) help cognitive symptoms in mild to moderate Alzheimer disease; memantine (5 to 20 mg) is for moderate to severe disease.
• Non-drug interventions (cognitive stimulation, carer support, meaningful activity) are foundational.
• Antipsychotics are reserved for severe, dangerous or highly distressing agitation/psychosis, after non-drug measures, started low and reviewed, tapered if no response at 4 weeks, attempted withdrawal within 4 months, with monthly monitoring and 4 more months after stopping.
• Capacity and safety (driving, finance, medicines, falls, abuse) are central tasks and must be planned early.
• Risk reduction is lifelong and vascular-first.