Alzheimer's Disease: Causes, Symptoms and Treatment

Alzheimer's Disease: Causes, Symptoms and Treatment

Alzheimer's disease (AD) is the most common form of dementia, and affects memory and other cognitive abilities. It is a progressive, neurodegenerative disorder that destroys memory and cognitive function over years to decades — ultimately impairing the ability to carry out the simplest tasks of daily living.

Alzheimer's disease places a substantial burden on people living with dementia and their carers. Population estimates depend on the year and definition; this guide does not present an undated prevalence estimate as current.

What Causes Alzheimer's Disease?

Alzheimer's disease is characterised at the cellular level by two abnormal protein accumulations:

Amyloid Plaques

The amyloid precursor protein (APP) is cleaved by secretase enzymes. In Alzheimer's disease, abnormal cleavage produces a 42-amino-acid fragment called amyloid-β (Aβ42) that aggregates into oligomers and then forms insoluble plaques that accumulate outside neurons in the brain. These amyloid plaques disrupt synaptic transmission and trigger neuroinflammation.

The amyloid cascade hypothesis proposes that amyloid accumulation is the initiating event, occurring 10–20 years before symptoms appear. This has driven the development of anti-amyloid therapies.

Tau Neurofibrillary Tangles

Tau is a protein that normally stabilises the internal scaffolding (microtubules) that transport nutrients within neurons. In Alzheimer's disease, tau becomes hyperphosphorylated, detaches from microtubules, and aggregates into twisted tangles (neurofibrillary tangles — NFTs) inside neurons. NFTs spread through the brain in a stereotyped pattern (Braak stages), correlating with cognitive decline.

Neuronal Death and Brain Atrophy

The combined effect of plaques, tangles, and neuroinflammation leads to synaptic dysfunction and progressive neuronal death — particularly in the hippocampus (memory) and entorhinal cortex initially, then spreading to the temporal, parietal, and frontal cortices. Brain atrophy develops as the disease progresses.

Risk Factors

Age is an important risk factor, but dementia is not an inevitable part of ageing.

Genetics: APOE variants can influence risk without determining whether someone will develop Alzheimer's. Certain variants in APP, PSEN1 and PSEN2 are associated with rare inherited forms. The meaning of a result depends on the specific variant and family history; discuss testing and its implications with a specialist or genetic counsellor.

Other risk factors: cardiovascular risk factors (hypertension, diabetes, obesity, dyslipidaemia, smoking) — "what is bad for the heart is bad for the brain"; head trauma (particularly repeated or severe); social isolation; hearing loss; low educational attainment (reduced cognitive reserve); depression.

Protective factors: higher education, cognitive engagement, regular aerobic exercise, Mediterranean diet, social connection.

Stages and Symptoms

Alzheimer's disease progresses through recognisable stages, though the rate varies.

Changes Before Symptoms

Biological changes can precede symptoms by years. Biomarker tests may include PET imaging, cerebrospinal fluid tests and, in appropriate clinical settings, blood tests. A test result alone does not establish a treatment indication. Research in people without symptoms should not be confused with eligibility for an approved medicine.

Mild Cognitive Impairment (MCI) Due to Alzheimer's

The transitional stage between normal cognition and dementia. The individual notices memory difficulties that others can also observe, but daily function remains largely intact.

Symptoms:

• Forgetting recent events, conversations, or appointments
• Difficulty retaining new information
• Mild word-finding difficulty
• Navigational difficulties in new environments

Some people with MCI develop dementia, while others do not. MCI has several possible causes and needs individual assessment.

Mild Alzheimer's Dementia

Memory loss now affects daily life. Family members notice significant changes.

• Repeatedly asking the same questions; forgetting recent conversations
• Getting lost in familiar places
• Difficulty managing finances, planning, or complex tasks
• Personality changes — increased anxiety, withdrawal, irritability, apathy
• Word-finding difficulties; circumlocution (talking around words)

Moderate Alzheimer's Dementia

The person requires assistance with daily activities.

• Unable to recall the names of close family members
• Forgetting personal history (address, phone number, where they were born)
• Confusion about time, day, month, year, and season
• Behavioural symptoms: agitation, wandering, suspicion or paranoia, sleep disturbance, aggression
• Difficulty with dressing, hygiene, and toileting
• Hallucinations (less common than in Lewy body dementia but can occur)

Severe Alzheimer's Dementia

Complete dependence on care.

• Loss of verbal communication — only short phrases or single words
• Inability to perform any activities of daily living (eating, dressing, toileting, bathing)
• Bladder and bowel incontinence
• Loss of mobility — ultimately confined to bed
• Highly susceptible to infections (aspiration pneumonia is the most common cause of death)

Diagnosis

Clinical Assessment

Assessment combines the person's and family's history, cognitive and functional evaluation, and appropriate investigations. Biomarkers may contribute to diagnosis in selected cases. The neurologist or geriatrician assesses:

• Pattern of cognitive deficits (episodic memory loss is the hallmark)
• Onset, progression, and functional impact
• Medications, medical history, and vascular risk factors
• Depression and other reversible causes of cognitive impairment

Cognitive tests: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Addenbrooke's Cognitive Examination (ACE) — standardised tools to quantify and track cognitive deficits.

Neuropsychological testing — formal, detailed assessment of memory domains, executive function, language, visuospatial skills, and attention to characterise the pattern and severity of impairment.

Brain Imaging

MRI of the brain may help assess structural changes and other possible causes of symptoms. Findings can include:

• Disproportionate hippocampal and medial temporal lobe atrophy
• Cortical atrophy in temporal and parietal regions
• White matter changes (leukoaraiosis) reflecting vascular burden
• Findings suggesting another or additional cause, such as a tumour, prior stroke or hydrocephalus

Amyloid PET scan assesses amyloid deposits. The specialist interprets the result with symptoms, other tests and the clinical context; it should not be presented as a standalone guarantee that all causes of cognitive impairment have been confirmed or excluded.

FDG-PET — shows hypometabolism in temporal and parietal cortex; useful for distinguishing AD from other dementias.

Biomarker Testing

Cerebrospinal fluid (CSF) biomarkers — obtained by lumbar puncture:

• Low Aβ42 (amyloid being sequestered in plaques)
• High tau and phospho-tau (reflecting neurodegeneration and tangle formation)
• The "Alzheimer's CSF signature" has high diagnostic accuracy

Blood biomarkers can contribute to evaluation when an appropriate validated test is available. NIA advises that blood-test results alone should not diagnose dementia. Test selection and interpretation belong with the clinical assessment; availability and regulatory indications vary.

Treatment

Currently Approved Symptomatic Treatments

No treatment currently reverses or halts Alzheimer's disease progression. Symptomatic treatments modestly improve cognitive function and delay functional decline.

Cholinesterase inhibitors — donepezil (Aricept), rivastigmine, galantamine. Block the breakdown of acetylcholine, a neurotransmitter deficient in AD. Provide modest cognitive and functional benefit in mild-to-moderate AD. The authorised indication for each medicine depends on the jurisdiction and product. Side effects: nausea, diarrhoea, bradycardia.

Memantine — blocks overactivation of NMDA glutamate receptors, which contributes to excitotoxic neuronal death. Used for selected patients with moderate-to-severe disease under the applicable prescribing information. Often combined with a cholinesterase inhibitor. Modest benefit; good tolerability.

Disease-Modifying Therapy — Anti-Amyloid Antibodies

A major milestone in Alzheimer's treatment came with the approval of anti-amyloid monoclonal antibodies that remove amyloid plaques from the brain:

Lecanemab (Leqembi) and donanemab (Kisunla) have US FDA authorisations for Alzheimer's disease, with treatment initiated in the mild cognitive impairment or mild dementia stages described in their prescribing information. They target amyloid and can slow decline in selected patients; they are not cures. Confirmation of amyloid pathology and a specialist assessment are required.

These medicines can cause amyloid-related imaging abnormalities (ARIA), including brain swelling and bleeding. Serious events can occur. Candidate selection, discussion of genetic and other risk factors, and MRI monitoring are essential. Follow the current product-specific label and treating service for route, schedule, monitoring and any decision to stop.

US authorisation does not establish Chinese approval, local supply, personal eligibility or reimbursement. This article does not recommend treatment for an asymptomatic person or promise access to either medicine in China.

Non-Pharmacological Management

• Cognitive and social activities — discuss suitable, enjoyable activities with the care team
• Physical activity — plan safe activity suited to ability, health and preferences
• Occupational therapy — home adaptations, daily routine structure, carer training
• Behavioural and psychological symptom management: non-pharmacological approaches first; low-dose antipsychotics only for severe agitation/psychosis with clear risk-benefit assessment
• Carer support — education, respite care, and psychological support for family carers, who carry the greatest burden of AD

Dementia and Alzheimer's Care in China

Before travel, ask the receiving memory service about clinical assessment, cognitive testing and which investigations are indicated and available. Do not assume that MRI, PET, CSF or blood biomarkers are all needed or that every centre provides them.

Ask the specialist whether any disease-modifying therapy is appropriate and what the local authorisation, supply, monitoring and continuing-care requirements are. Confirm an itemised quote and separate coordination scope. A multidisciplinary plan may involve medical, rehabilitation and carer support, but the actual services and languages must be confirmed with the providers. Confirm timing and treatment access with the institution; comparative prices are not established here.

Contact a PriumCare care navigator to arrange a memory and cognitive assessment, Alzheimer's disease evaluation, or second opinion on dementia diagnosis.

Sources and editorial correction

• NIA: Alzheimer’s diagnosis.
• NIA: causes and genetics.
• FDA: Kisunla approval.
• FDA: Leqembi MRI safety monitoring.

Editorial source correction: 25 October 2026. This check addressed biomarker and exclusion claims, genetic certainty, undated population estimates, drug-schedule and eligibility wording, and unsupported service and comparative-cost claims. It is not a clinical review of the whole article and does not certify an individual treatment plan. No named medical reviewer is claimed. Original publication date is retained.