Dementia — Types, Causes, Alzheimer's Disease & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Dementia is an umbrella term for a group of conditions characterised by progressive decline in multiple cognitive domains — including memory, language, executive function, attention, and visuospatial ability — severe enough to impair daily functioning and independent living. It is not a normal part of ageing. The most common types are Alzheimer's disease (AD, 60-70% of cases — characterised by amyloid plaques and neurofibrillary tau tangles); vascular dementia (VaD, 15-20% — caused by cerebrovascular disease including stroke and small vessel disease); Lewy body dementia (LBD, 10-15% — featuring alpha-synuclein inclusions, visual hallucinations, and parkinsonism); frontotemporal dementia (FTD, 5-10% — prominent personality change and executive dysfunction, earlier onset); and mixed dementia (AD plus VaD — very common in the elderly). Dementia affects 57 million people globally and represents a major public health crisis projected to affect 153 million by 2050.

Alzheimer's disease is caused by accumulation of amyloid-beta plaques and neurofibrillary tau tangles leading to neuronal death. The strongest genetic risk factor is APOE epsilon-4 allele (heterozygous 2-3x risk; homozygous 8-12x risk). Rare autosomal dominant mutations in APP, PSEN1, and PSEN2 genes cause early-onset familial AD (below 65 years) in under 1% of cases. Down syndrome (trisomy 21) predisposes to AD by age 40-50 due to an extra copy of the APP gene. The Lancet 2024 Dementia Prevention Commission identified 14 modifiable risk factors accounting for approximately 45% of dementia cases: low education, midlife hypertension, hearing loss, smoking, obesity, depression, physical inactivity, diabetes, low social contact, excessive alcohol, traumatic brain injury, air pollution, high LDL cholesterol, and untreated vision loss. Vascular dementia risk factors parallel cardiovascular risk: hypertension, diabetes, atrial fibrillation, hyperlipidaemia, and smoking. Lewy body dementia has a strong genetic component with SNCA and GBA variants identified.

Early Alzheimer's disease: short-term memory loss (forgetting recent conversations, appointments, and names while remote memories remain preserved); getting lost in familiar places; word-finding difficulties (anomia — searching for words mid-sentence); difficulty with complex tasks such as managing finances or planning; and personality or mood changes including anxiety, depression, and social withdrawal. As AD progresses: significant memory loss, disorientation to time and place, agitation and wandering, sundowning (worsening confusion in the evening), and need for assistance with personal care. Severe AD: inability to recognise family members, incontinence, minimal verbal communication, and swallowing difficulties (dysphagia). Lewy body dementia: vivid detailed visual hallucinations (people or animals, well-formed), REM sleep behaviour disorder (acting out dreams — often precedes cognitive decline by years), parkinsonism, and marked fluctuating cognition. Vascular dementia: stepwise decline following stroke or TIAs, focal neurological deficits, and prominent executive dysfunction with relatively preserved memory in some cases.

Clinical history from patient and carer is essential: documenting the onset, progression, and pattern of cognitive and functional decline. Cognitive assessment tools: Mini-Mental State Examination (MMSE — useful but insensitive for mild dementia); Montreal Cognitive Assessment (MoCA — more sensitive for mild cognitive impairment); ACE-III (Addenbrooke's Cognitive Examination — comprehensive multi-domain assessment). Brain MRI: standard — assesses hippocampal atrophy (characteristic of AD), cerebrovascular disease (VaD), structural causes (tumour, normal pressure hydrocephalus, subdural haematoma), and white matter changes. Blood tests exclude reversible causes: thyroid function (hypothyroidism), vitamin B12 and folate, FBC, renal function, liver function, calcium, glucose, and syphilis serology in appropriate populations. CSF biomarkers (amyloid-42/40 ratio, phosphorylated tau, total tau) in specialist settings confirm AD pathology and guide eligibility for anti-amyloid therapies. Amyloid PET scan: detects amyloid plaque deposition, used in clinical trials and specialist dementia clinics. APOE genotyping for familial AD risk assessment.

Cholinesterase inhibitors for Alzheimer's disease: donepezil (Aricept — 5 mg for one month then 10 mg daily; also 23 mg for advanced AD), rivastigmine (Exelon — also approved for Parkinson's disease dementia; available as 9.5 mg/24hr transdermal patch reducing GI side effects), and galantamine (Reminyl — also has nicotinic receptor modulating activity). These inhibit acetylcholinesterase, increasing acetylcholine availability in the brain. They modestly slow cognitive and functional decline in mild-moderate AD but do not reverse or halt neurodegeneration. Memantine (Ebixa): NMDA glutamate receptor antagonist, approved for moderate-severe AD; modest benefit on cognition, behaviour, and activities of daily living; can be combined with donepezil. Anti-amyloid disease-modifying therapies: lecanemab (Leqembi) — Phase III CLARITY AD trial showed 27% slowing of clinical decline at 18 months in early AD (MCI/mild dementia with confirmed amyloid pathology); approved by FDA (2023) and NICE (2025); given IV fortnightly; risk of ARIA (amyloid-related imaging abnormalities — brain microbleeds/oedema in 21%). Donanemab (Kisunla) — similar efficacy, FDA approved 2024. Non-pharmacological: cognitive stimulation therapy (CST), structured aerobic exercise, social engagement, reminiscence therapy, and carer education. Antipsychotics (risperidone) only for severe behavioural symptoms causing risk — increases mortality and stroke risk in dementia.

Advanced dementia causes complete loss of independence — patients cannot dress, eat, toilet, or communicate. Aspiration pneumonia from swallowing difficulty accounts for approximately 70% of end-stage dementia deaths. Urinary tract infections, malnutrition, pressure ulcers, and contractures affect immobile patients. Wandering causes falls, injuries, and hypothermia. Delirium (acute confusion) from intercurrent illness accelerates cognitive decline and carries high short-term mortality in dementia patients. Hospitalisation rates are 3-5 times higher than in cognitively normal elderly patients. Behavioural and psychological symptoms (aggression, psychosis, agitation) are the primary drivers of care home admission and carer breakdown. Family and carer psychological distress and burnout affect up to 70% of dementia caregivers.

The Lancet 2024 Commission identified that 45% of dementia cases may be prevented by addressing modifiable risk factors. Physical activity: 150 minutes per week of moderate aerobic exercise reduces dementia risk by 35% — one of the most powerful evidence-based interventions. Treat midlife hypertension aggressively (SPRINT-MIND trial: intensive BP control to below 120 mmHg reduced MCI risk by 19%). Address hearing loss with hearing aids — hearing loss is the largest modifiable risk factor in midlife, accounting for 9% of potentially preventable dementia. Smoking cessation reduces dementia risk within 5 years of quitting. Mediterranean and MIND diets (emphasising leafy greens, berries, nuts, olive oil, fish) are associated with 35-53% reduced dementia risk. Maintain social connections, pursue cognitively stimulating leisure activities, and aim for higher educational attainment. Control cardiovascular risk factors — hypertension, hyperlipidaemia, and diabetes are the most actionable risk factors for prevention. Adequate sleep (7-8 hours): sleep deprivation accelerates amyloid accumulation.

Seek medical assessment if you or a family member notices: persistent short-term memory loss that is worsening over months; getting lost in familiar places; difficulty managing finances, bills, or complex daily tasks; significant personality changes, increasing suspicion, or apathy; word-finding difficulties affecting conversation; or a carer or family member repeatedly expressing concern about your memory or behaviour. Early assessment is important — diagnosis allows access to treatments (cholinesterase inhibitors, newer anti-amyloid therapies), safety planning, driving assessment, legal and financial planning while capacity is preserved, and access to carer support. Many reversible causes of cognitive impairment (hypothyroidism, B12 deficiency, normal pressure hydrocephalus, depression) can be identified and treated. A GP can arrange initial assessment and refer to a memory clinic or specialist.