Dementia: cognitive assessment, treatment options, and coordinated care in AU

Dementia — the second leading cause of death in Australia

Dementia describes progressive, irreversible decline in cognition across at least two domains — memory, executive function, language, visuospatial ability, or behaviour — severe enough to interfere with independent daily activities. It is not a single disease but a syndrome with multiple underlying causes.

Approximately 470,000 Australians live with dementia, making it the second leading cause of death nationally (Dementia Australia). Numbers are expected to rise as the population ages. Alzheimer’s disease accounts for ~60% of cases, vascular dementia for ~20%, and mixed pathology (Alzheimer’s plus vascular) is increasingly recognised as the most common presentation in older adults. Lewy body dementia and frontotemporal dementia are the next most common subtypes.

General practice holds a pivotal role: cognitive case-finding in older patients and those with relevant symptoms, reversible-cause exclusion, referral for diagnosis and imaging, coordinating pharmacological and non-pharmacological management, advance care planning, carer support, and navigating the aged care system — all before and after specialist input.

A. Core clinical — the AU general-practice framework

Reversible and contributing causes — exclude first

Before attributing cognitive decline to neurodegenerative dementia, eTG and RACGP emphasise ruling out:

• Depression (pseudodementia) — depression in older adults commonly mimics dementia; treat the depression and reassess cognition
• Hypothyroidism — TSH is mandatory in any cognitive workup
• B12 and folate deficiency — particularly in older adults on restricted diets, on metformin, or after gastric surgery
• Vitamin D deficiency — associated with cognitive function; treat if less than 50 nmol/L
• Medications — anticholinergic burden (opioids, tricyclics, oxybutynin, older antihistamines, certain antidepressants), benzodiazepines, sedating antidepressants, valproate; review every medication systematically
• Alcohol — chronic alcohol-related brain damage and Korsakoff syndrome
• Obstructive sleep apnoea — disrupts sleep architecture and impairs cognition; STOP-BANG screen
• Hearing and vision loss — both are significant and modifiable per Lancet Commission 2024; hearing aid provision alone reduces dementia risk in high-risk groups
• Normal pressure hydrocephalus (NPH) — gait apraxia + cognitive impairment + urinary incontinence; potentially reversible with VP shunt
• Subdural haematoma — head injury or anticoagulation; CT brain required

Cognitive assessment tools

RACGP guidance on cognitive screening:

• MoCA (Montreal Cognitive Assessment) — /30; most sensitive for mild cognitive impairment and early dementia; preferred over MMSE for case-finding; free for clinical use; education correction required (add 1 point for ≤12 years education)
• MMSE — /30; less sensitive for MCI; still widely used; copyright restrictions limit routine use
• Mini-Cog — 3-word recall + clock draw; under 5 minutes; useful when time is limited
• RUDAS — culturally adapted; preferred for Aboriginal and Torres Strait Islander patients and those from non-English-speaking backgrounds
• IQCODE / AD-8 informant interview — collateral history from partner or family member is essential; often more sensitive than direct testing in early disease

A cognitive screen is incorporated within the MBS 75+ health assessment (item 705), 45-to-49-year assessment (item 701 — for modifiable risk reduction), and ATSI health assessment (item 715 — using RUDAS or KICA).

Investigations

• FBC, U&E, eGFR, calcium, glucose/HbA1c, TFT, B12, folate, vitamin D — mandatory first-line
• Urinalysis — exclude UTI-related acute confusion
• CT brain — standard of care; excludes structural causes (tumour, NPH, subdural haematoma, large vessel stroke)
• MRI brain — more detailed; medial temporal lobe atrophy in Alzheimer’s; small vessel changes in vascular dementia; specialist-ordered
• Specialist-led: neuropsychological testing, amyloid/tau PET, CSF biomarkers (Aβ42 ratio, p-tau), plasma p-tau217 (emerging clinical utility, specialist only in 2026)

B. Dementia subtypes and treatment

Alzheimer’s disease

The most common subtype; insidious onset; episodic memory most impaired early (cannot retain new information); hippocampal atrophy on MRI. Pathologically: amyloid-beta plaques and neurofibrillary tau tangles.

Pharmacotherapy:

Cholinesterase inhibitors (ChEI) — donepezil, rivastigmine (also available as a patch), galantamine — per AMH and eTG:

• PBS Authority Required for mild-to-moderate Alzheimer’s disease (baseline MMSE approximately 10–24)
• Also appropriate (off-label PBS, private script) for Lewy body dementia and Parkinson’s dementia
• Benefit: modest cognitive stabilisation and ADL improvement over 6–12 months; NNT ~10 for meaningful ADL benefit
• Side effects: nausea, diarrhoea, vivid dreams, bradycardia and syncope (caution in AV block, sick sinus syndrome, low resting heart rate)
• Titrate slowly: donepezil 5 mg nocte → 10 mg after 4 weeks; rivastigmine patch 4.6 mg/24h → 9.5 mg/24h; galantamine PR 8 → 16 → 24 mg daily

Memantine — NMDA-receptor antagonist; PBS Authority for moderate-to-severe Alzheimer’s (MMSE typically ≤14); modest benefit for cognition and behavioural symptoms; well tolerated; titrate 5 → 20 mg daily.

Anti-amyloid monoclonal antibodies — lecanemab (Leqembi, TGA-registered September 2025) and donanemab (Kisunla, TGA-registered May 2025) are the first disease-modifying agents for Alzheimer’s disease:

• Indicated for MCI or mild Alzheimer’s with confirmed amyloid on biomarker (PET or CSF)
• Specialist-initiated; IV infusion every 2–4 weeks; mandatory serial MRI to monitor for ARIA (amyloid-related imaging abnormalities — oedema or microhaemorrhage)
• APOE4 homozygotes are excluded from donanemab eligibility due to very high ARIA risk
• Modest clinical effect (~25–35% slowing on CDR-SB scale)
• Not PBS-listed in 2026 — private access only at ~AUD $80,000–100,000/year; PBAC consideration ongoing

Vascular dementia

Stepwise or gradual decline related to cerebrovascular disease; gait disturbance, executive dysfunction, and focal neurological signs may be present. Management is aggressive vascular risk reduction: blood pressure target less than 130/80 mmHg, statin per cardiovascular risk, antiplatelet therapy post-stroke, smoking cessation, and blood glucose optimisation in diabetes. ChEIs are not PBS-listed for pure vascular dementia.

Lewy body dementia (DLB)

Fluctuating cognition, recurrent well-formed visual hallucinations, spontaneous parkinsonism, and REM sleep behaviour disorder are the cardinal features. Critical: avoid antipsychotic medications — severe neuroleptic sensitivity reactions (acute parkinsonism, hyperthermia, reduced consciousness, death) occur. If an antipsychotic is unavoidable, quetiapine 12.5–25 mg is lowest risk. ChEIs are first-line pharmacotherapy; melatonin for REM sleep behaviour disorder.

Frontotemporal dementia (FTD)

Earlier onset, typically 50–65 years; personality change, disinhibition, apathy, and hyperorality in the behavioural variant; progressive language impairment in the language variants. No disease-modifying treatment; management is symptom-focused and carer-education intensive. Genetic counselling relevant for familial forms (MAPT, GRN, C9ORF72).

C. Behavioural and psychological symptoms — BPSD

RACGP Silver Book BPSD chapter positions non-pharmacological approaches as first-line for all behavioural symptoms:

1. Identify and address precipitants: pain (use Abbey Pain Scale in non-verbal patients), constipation, urinary tract infection, hypoxia, hearing aid or glasses not worn, unmet needs (thirst, loneliness, boredom), environmental change, carer distress
2. Non-pharmacological bundle: person-centred care, structured activity, personalised music playlists, validation therapy, reminiscence, familiar environment, dementia-friendly design, carer education

When pharmacological treatment is unavoidable for severe distress, psychosis, or aggression where there is risk of harm:

• Risperidone — the only PBS-listed antipsychotic for Alzheimer’s-type BPSD; Authority Required; maximum 12 weeks; 0.25 mg twice daily, max 1 mg twice daily; TGA restricted to severe psychosis or persistent aggression in Alzheimer’s
• All antipsychotics carry TGA/FDA black-box warning: increased mortality (~1.6–1.7× risk) and stroke in dementia; reserve for genuine safety risk
• SSRIs (sertraline, citalopram) for depression or anxiety in dementia; avoid paroxetine (high anticholinergic burden)
• Avoid benzodiazepines — worsen confusion, increase falls, cause paradoxical disinhibition

D. Australian operations

MBS items for dementia management:

Standard consultations (items 23, 36, 44 — item 44 is appropriate for lengthy cognitive assessment or advance care planning discussions). 75+ health assessment (item 705, or 707 for prolonged) includes a mandatory cognitive component. Telehealth items (92027–92029 video; 92060 phone) apply for follow-up and BPSD management discussions, with the 12-month existing-relationship requirement; in-person is preferred for initial cognitive assessment.

GP Chronic Condition Management Plan (GPCCMP — items 965/967) is appropriate for established dementia and enables Allied Health referrals: occupational therapist (home modifications, ADL strategies), exercise physiologist (falls and strength), dietitian, physiotherapy, speech pathologist (dysphagia), podiatry. Mental Health Care Plan (items 2715/2717) applies when comorbid depression or anxiety are present — dementia itself does not qualify, but its frequent comorbidities do.

PBS medications:

• ChEIs (donepezil, rivastigmine, galantamine) — PBS Authority Required (combined initial/continuing phases since May 2023); mild-to-moderate Alzheimer’s
• Memantine — PBS Authority Required; moderate-to-severe Alzheimer’s; cannot be co-prescribed with ChEI on PBS (private script if combining)
• Risperidone for BPSD — PBS Authority Required; 12-week restriction; only PBS-listed antipsychotic for BPSD
• Anti-amyloid mAbs (lecanemab, donanemab) — not PBS-listed 2026; private/SAS access only

My Aged Care pathway (myagedcare.gov.au):

• Contact on 1800 200 422 or online to request an ACAT assessment
• Home Care Packages (levels 1–4) for community-based care; from 1 July 2025 replaced by Support at Home Program for new entrants
• Residential aged care when home support is no longer sufficient
• Veterans: DVA covers dementia care for eligible veterans
• Young-onset dementia (under 65): NDIS funding pathway

E. Special populations

Young-onset dementia (under 65). Frontotemporal dementia is disproportionately represented. Genetic counselling is relevant. NDIS eligibility for younger patients with dementia causing disability. Significant psychosocial and employment impacts require specific support — Dementia Australia has dedicated young-onset services.

Aboriginal and Torres Strait Islander peoples. Dementia prevalence is higher and onset earlier in Aboriginal and Torres Strait Islander populations. The KICA (Kimberley Indigenous Cognitive Assessment) and RUDAS are culturally appropriate assessment tools. The ATSI health assessment (item 715) provides the opportunity for formal cognitive screening. Community-appropriate communication and involvement of family in care planning are essential.

Drivers with dementia. Driving assessment follows Austroads Assessing Fitness to Drive 2022 standards. Occupational therapy driving assessment is required for borderline or disputed cases — cognitive testing alone is insufficient. Mandatory reporting applies in the Northern Territory and South Australia; ethical reporting obligations apply elsewhere. Driving cessation is distressing and should be planned with the patient and family proactively while capacity remains.

Advance care planning while capacity is preserved. The most important time-sensitive GP task in early dementia is initiating advance care planning: Enduring Power of Attorney (financial), Enduring Guardianship (health decisions), and an Advance Care Directive. These lose legal validity if the person no longer has capacity to execute them. Advance Care Planning Australia has jurisdiction-specific resources.

When to escalate

Refer to the emergency department for: acute severe behavioural disturbance with risk of harm to patient or others, delirium superimposed on dementia with medical cause requiring investigation, or sudden marked cognitive deterioration (subdural haematoma, stroke, encephalitis, metabolic crisis).

Geriatric medicine, psychogeriatric, or neurology specialist referral for: initial diagnosis when uncertain, young-onset dementia, rapidly progressive decline, complex BPSD requiring specialist medication management, assessment for anti-amyloid mAb candidacy, and contested capacity or driving decisions.

Routine referral: annual review with geriatric medicine or psychogeriatrics where available; neuropsychological testing for detailed cognitive profiling.

What this article is and is not

This is general health information drawn from Dementia Australia, CDPC guidelines, eTG, AMH, RACGP, NPS MedicineWise, TGA, and the Lancet Commission 2024. It is not personal medical advice and does not create a doctor–patient relationship. Diagnosis, medication decisions, and care planning should be made with your GP, geriatrician, or neurologist.

For support: Dementia Australia — National Dementia Helpline 1800 100 500. My Aged Care 1800 200 422. Carer Gateway 1800 422 737.

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Sources cited

1. Dementia Australia
2. Clinical Practice Guidelines for Dementia in Australia (CDPC)
3. RACGP — Dementia / Silver Book BPSD
4. Therapeutic Guidelines (eTG) — Psychotropic/Dementia
5. Australian Medicines Handbook
6. NPS MedicineWise — Anticholinergic burden
7. TGA — Leqembi (lecanemab) registration
8. Lancet Commission 2024 — Dementia prevention, intervention and care
9. My Aged Care
10. Advance Care Planning Australia
11. Austroads — Assessing Fitness to Drive 2022