Cassandra's Compass
Dementia Knowledge Hub
A unified, evidence-based resource covering dementia progression and stages, medical terminology, sleep and dementia, common conditions, new diagnosis guidance, and brain anatomy — APA referenced throughout.
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Dementia — Stages & Progression
Dementia stages and progression, all major types, and evidence-based care strategies for professionals, carers, and students — APA referenced throughout
There are over 100 causes of dementia. The following are the most clinically significant types relevant to Australian aged care practice. Each has a distinct neurological basis, symptom profile, and management approach. Accurate type identification significantly changes clinical management. For interactive brain anatomy, visit the Brain Lab.
Alzheimer's Disease
Pathology
Progressive accumulation of amyloid-beta plaques (extracellular) and neurofibrillary tau tangles (intracellular) causing neuronal death. Begins in the entorhinal cortex and hippocampus, spreading outward.
Onset Pattern
Typically gradual. Most common in those over 65 (late-onset). Early-onset (before 65) affects approximately 5–10% of cases.
Early Symptoms
Short-term memory loss — forgetting recent events, conversations
Asking the same question repeatedly
Word-finding difficulty (tip-of-tongue)
Difficulty with new learning
Getting lost in familiar places
Temporal disorientation — losing track of dates and time
Later Symptoms
Difficulty recognising family members
Severe language impairment — aphasia
Inability to manage all ADLs
Behavioural and psychological symptoms (BPSD)
Physical decline — dysphagia, incontinence, immobility
Medication & Treatment
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) — mild to moderate. Memantine — moderate to severe. Neither prevents progression but may temporarily slow decline.
APA Reference
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., ... & Sperling, R. (2018). NIA-AA research framework: Toward a biological definition of Alzheimer's disease. Alzheimer's & Dementia, 14(4), 535–562.
Vascular Dementia
Pathology
Cognitive impairment caused by reduced blood flow to the brain — either from large vessel strokes (post-stroke dementia) or, more commonly, small vessel disease (lacunar infarcts, white matter hyperintensities). Risk factors: hypertension, diabetes, smoking, atrial fibrillation, hypercholesterolaemia.
Onset Pattern
Often sudden (post-stroke) or stepwise — noticeable deterioration followed by plateau, then further deterioration. Some cases are gradual (small vessel disease).
Early Symptoms
Executive function impairment — planning, organising, sequencing
Slowed thinking and processing speed
Attention and concentration difficulties
Memory less severely affected than Alzheimer's early on
Gait disturbance (shuffling, broad-based)
Urinary urgency or incontinence appearing early
Later Symptoms
Progressive cognitive decline after each vascular event
Significant functional impairment
BPSD including depression, apathy, and emotional lability
Physical complications of underlying vascular disease
Medication & Treatment
No specific medications approved for vascular dementia. Management focuses on reducing further vascular events: antihypertensives, antiplatelets, statins, diabetes management, anticoagulation (if atrial fibrillation). Lifestyle modification is essential.
APA Reference
O'Brien, J. T., & Thomas, A. (2015). Vascular dementia. The Lancet, 386(10004), 1698–1706.
Lewy Body Dementia (DLB)
Pathology
Abnormal accumulation of alpha-synuclein protein (Lewy bodies) in neurons of the brainstem, limbic system, and cortex. Overlaps significantly with Parkinson's disease dementia (PDD) — Lewy body disease is a spectrum.
Onset Pattern
Typically gradual. Key distinguishing features help differentiate from Alzheimer's: REM sleep behaviour disorder often precedes cognitive symptoms by years.
Early Symptoms
Fluctuating cognition — noticeable day-to-day variability
Well-formed, detailed visual hallucinations (people, animals)
Parkinsonism — tremor, rigidity, bradykinesia, shuffling gait
REM sleep behaviour disorder — physically acting out dreams
Repeated falls and syncope (loss of consciousness)
Autonomic dysfunction — blood pressure fluctuation, constipation, urinary problems
Later Symptoms
Severe cognitive impairment
Significant Parkinsonism
Frequent falls and injury
Severe autonomic instability
Worsening visual hallucinations and paranoid delusions
Medication & Treatment
⚠️ CRITICAL SAFETY ALERT: Antipsychotics — both conventional (such as haloperidol) and atypical (including olanzapine and risperidone) — carry a severe risk in DLB and can cause life-threatening neuroleptic sensitivity reactions including irreversible severe Parkinsonism, reduced consciousness, and death. None should be started, stopped or changed without specialist review. If antipsychotics are required, only quetiapine (at very low doses) or clozapine under specialist guidance. Cholinesterase inhibitors (rivastigmine patch) are first-line cognitive treatment.
APA Reference
McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J. P., Weintraub, D., ... & Kosaka, K. (2017). Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium. Neurology, 89(1), 88–100.
Frontotemporal Dementia (FTD)
Pathology
Progressive degeneration of the frontal and temporal lobes. Several subtypes: behavioural variant FTD (bvFTD — frontal lobe dominant), semantic variant primary progressive aphasia (svPPA — left temporal), non-fluent variant PPA (nfvPPA). Pathologically heterogeneous — may involve TDP-43, tau, or FUS protein inclusions.
Onset Pattern
Typically younger onset (50s–60s). Often misdiagnosed as depression, bipolar disorder, midlife crisis, or personality disorder because memory is relatively preserved early while behaviour is markedly changed.
Early Symptoms
Personality change — previously reserved person becomes disinhibited, impulsive
Loss of social awareness and empathy (behavioural variant)
Socially inappropriate behaviour — saying offensive things, touching strangers
Dietary changes — carbohydrate craving, overeating, oral fixation
Compulsive, repetitive behaviours (rituals, collecting objects)
Language difficulties (semantic/non-fluent variants)
Memory relatively preserved early — often the biggest diagnostic clue
Later Symptoms
Profound behavioural impairment
Physical function may remain relatively preserved
Mutism in language variants
Parkinsonism may develop
Medication & Treatment
No approved disease-modifying treatments. Cholinesterase inhibitors are NOT effective in FTD and may worsen behavioural symptoms. SSRIs may help behavioural symptoms (disinhibition, compulsions) — under specialist guidance. Antipsychotics may be used cautiously for severe aggression.
APA Reference
Rascovsky, K., Hodges, J. R., Knopman, D., Mendez, M. F., Kramer, J. H., Neuhaus, J., ... & Miller, B. L. (2011). Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia. Brain, 134(9), 2456–2477.
Parkinson's Disease Dementia (PDD)
Pathology
Alpha-synuclein (Lewy body) pathology — same pathological mechanism as DLB, but motor symptoms (tremor, rigidity, bradykinesia) preceded cognitive symptoms by more than 1 year (the "1-year rule" distinguishes PDD from DLB). Part of the Lewy body disease spectrum.
Onset Pattern
Cognitive decline emerges typically 10–15 years after Parkinson's motor symptom onset.
Early Symptoms
Executive function impairment (planning, sequencing)
Slowed thinking (bradyphrenia)
Attention and concentration difficulties
Visuospatial difficulties
Existing motor features worsen
Hallucinations (often medication-related initially)
Later Symptoms
Progressive cognitive decline alongside worsening Parkinsonism
Falls risk is extreme — both cognitive and physical causes
Dysphagia — aspiration pneumonia is common cause of death
Autonomic failure — postural hypotension, constipation, urinary problems
Medication & Treatment
Rivastigmine (Exelon) is specifically approved for PDD. CRITICAL: Antipsychotics that worsen Parkinsonism are highly problematic — same cautions as DLB. Clozapine or quetiapine only if absolutely necessary under specialist guidance.
APA Reference
Emre, M., Aarsland, D., Brown, R., Burn, D. J., Dunn, E. F., Lauritzen, M., ... & Zenner, H. P. (2007). Clinical diagnostic criteria for dementia associated with Parkinson's disease. Movement Disorders, 22(12), 1689–1707.
Young Onset Dementia (YOD)
Pathology
Young onset dementia is defined by age at onset (under 65), not by pathological type. The most common subtypes in young onset: Alzheimer's disease (genetic and sporadic), FTD (most common under 50), vascular, and Lewy body. Genetic mutations (PSEN1, PSEN2, APP for familial Alzheimer's; C9orf72, MAPT, GRN for FTD) are more frequently identified in younger onset cases.
Onset Pattern
Can occur in the 30s, 40s, or 50s — often initially attributed to stress, menopause, depression, or burnout, causing diagnostic delays averaging 4–8 years.
Early Symptoms
Often presents with non-memory symptoms — executive dysfunction, behaviour change, language difficulties
Significant impact on employment — person is often still working at diagnosis
Children at home — family devastation
Financial pressure — mortgage, dependent children, loss of income
May still drive — complex safety and legal considerations
Social isolation — peers do not understand dementia at this age
Later Symptoms
Same trajectory as the specific dementia type
Particularly devastating given young age and family context
Carers are usually a partner/spouse managing children and work simultaneously
Medication & Treatment
Depends on the specific dementia type. Genetic counselling should be offered. Carer support is critical — Dementia Australia Young Onset Dementia services (1800 100 500) are specifically tailored.
APA Reference
Hornberger, M., & Piguet, O. (2012). Episodic memory in frontotemporal dementia: A critical review. Brain, 135(3), 678–692. Dementia Australia. (2024). Young onset dementia. https://www.dementia.org.au/about-dementia/causes-and-types-dementia
Korsakoff Syndrome
Caused by severe thiamine (Vitamin B1) deficiency, almost always from chronic alcohol misuse. Characterised by anterograde amnesia, confabulation, and relatively preserved other cognitive functions. Partially reversible if thiamine is replaced early. Wernicke's encephalopathy is the acute precursor.
Posterior Cortical Atrophy (PCA)
A variant of Alzheimer's disease predominantly affecting the occipital and parietal lobes. Presents with progressive visual processing deficits (difficulty reading, judging distances, spatial awareness) while memory is relatively preserved. Often misdiagnosed or significantly delayed in diagnosis.
Creutzfeldt-Jakob Disease (CJD)
A rare, rapidly progressive, and invariably fatal prion disease. Characterised by rapidly progressive dementia, myoclonus (involuntary muscle jerks), ataxia, and death usually within 12 months of symptom onset. Variant CJD (vCJD) is linked to bovine spongiform encephalopathy (BSE).
Normal Pressure Hydrocephalus (NPH)
Accumulation of cerebrospinal fluid in the brain ventricles causing the classic triad: gait disturbance ("magnetic gait"), urinary incontinence, and cognitive impairment. Important because it is one of the few potentially reversible causes of dementia — ventriculoperitoneal shunting can be effective.
HIV-Associated Neurocognitive Disorder (HAND)
Cognitive impairment caused by HIV infection affecting the central nervous system. In the era of effective antiretroviral therapy, severe dementia is less common, but mild cognitive impairment remains prevalent in people living with HIV.
Dementia in Down Syndrome
Almost all people with Down syndrome (trisomy 21) who live to their 50s will develop Alzheimer's disease — the APOE4 gene mechanism and amyloid overproduction from the extra chromosome 21 create this near-universal risk. Baseline cognitive assessment in early adulthood is best practice.
Dementia Australia. (2024). Causes and types of dementia. https://www.dementia.org.au/about-dementia/causes-and-types-dementia | American Psychiatric Association. (2022). DSM-5-TR — Major and mild neurocognitive disorders. APA.
Related clinical resources across Cassandra's Compass
Educational content only. This hub consolidates evidence-based dementia resources — all citations conform to APA 7th Edition. © Cassandra's Compass 2026.
Knowledge is empowerment. The more you understand dementia, the more confidently — and compassionately — you can care.
— Cassandra's Compass
Verified against official sources on 2 October 2026