- Major Neurocognitive Disorder (MaND)
- The DSM-5-TR term for what most of the world continues to call "dementia." Involves significant cognitive decline from a prior level in one or more of the six cognitive domains — complex attention, executive function, learning/memory, language, perceptual-motor ability, and social cognition — that interferes with independence in everyday activities. ICD-11 retains the explicit "Dementia" category rather than renaming it. Both terminologies are current.
- Mild Neurocognitive Disorder (MiND)
- Modest cognitive decline that does not interfere significantly with daily independence. Overlaps substantially with the older term "mild cognitive impairment." Progression to MaND varies considerably: in memory-clinic samples the rate is often cited as ~10–15% per year, but population-based studies find lower rates and many individuals remain stable or revert to normal — particularly when the underlying cause is treatable (e.g., depression, medication effects, sleep disorder).
- Six DSM cognitive domains
- DSM-5-TR specifies six cognitive domains across which decline must be demonstrated: (1) Complex attention — sustained, divided, or selective attention; processing speed. (2) Executive function — planning, decision-making, working memory, inhibition. (3) Learning and memory — immediate and delayed recall, recognition. (4) Language — expressive and receptive; naming, fluency. (5) Perceptual-motor — visual construction, praxis, gnosis. (6) Social cognition — recognising emotions, theory of mind. Both MiND and MaND require documented decline in at least one domain; MaND requires it to interfere with independence.
- Normal ageing vs Mild vs Major NCD
- Normal ageing involves modest slowing of processing speed and some difficulty with effortful recall, but declarative memory, language, and daily function remain largely intact. Mild NCD involves a measurable decline from the person's own baseline — detected on neuropsychological testing — that does not impair daily independence. Major NCD involves functional impairment. Distinguishing normal ageing from Mild NCD requires longitudinal observation and neuropsychological assessment, not a single cross-sectional comparison with peers.
- Delirium
- An acute, fluctuating disturbance of attention and awareness arising from an underlying medical condition, substance intoxication/withdrawal, or medication. Onset is sudden (hours to days) and course fluctuates — cardinal features that distinguish it from dementia. Delirium is common in hospitalised older adults (20–30% of general medical inpatients; up to 50% post-surgery in the elderly) and carries significant mortality risk. It can be superimposed on existing dementia, making diagnosis more difficult. Unlike most neurocognitive disorders, delirium is often reversible if the underlying cause is identified and treated promptly.
- Mixed aetiology
- Post-mortem studies show that mixed pathology — typically Alzheimer's neuropathology co-occurring with cerebrovascular disease — is found in the majority of older adults with dementia. Pure single-aetiology dementia is less common than clinical diagnostic categories imply. The recognition of mixed dementia has therapeutic implications: vascular risk factor management may slow progression even in those with primary Alzheimer's pathology.
- Amyloid-beta (Aβ) plaques
- Extracellular deposits of misfolded amyloid-beta protein — a hallmark of Alzheimer's disease. The amyloid cascade hypothesis proposes that Aβ accumulation initiates a chain of events leading to neurodegeneration, though the relationship between plaques and symptoms is complex.
- Neurofibrillary tangles (tau)
- Intracellular aggregates of hyperphosphorylated tau protein, another neuropathological hallmark of Alzheimer's disease. Tau tangles correlate more closely with cognitive decline than amyloid plaques. Tauopathies (e.g., frontotemporal dementia) can occur independently of amyloid pathology.
- Lewy bodies
- Abnormal intracellular aggregates of alpha-synuclein protein found in neurons. The defining pathology of Dementia with Lewy Bodies (DLB) and Parkinson's disease dementia. Associated with four core diagnostic features per McKeith et al. (2017): fluctuating cognition, recurrent visual hallucinations, Parkinsonism, and REM sleep behaviour disorder.
- Cholinergic hypothesis
- The proposal that the cognitive symptoms of Alzheimer's disease result substantially from loss of cholinergic neurons in the basal forebrain (nucleus basalis of Meynert). This hypothesis underpins the use of acetylcholinesterase inhibitors (e.g., donepezil) as symptomatic treatments.
- Vascular dementia
- The second most common dementia, caused by cerebrovascular disease (strokes, small vessel disease, white matter lesions). Often shows a stepwise rather than gradual decline. Risk factors overlap with cardiovascular disease (hypertension, diabetes, smoking).
- Frontotemporal dementia (FTD)
- A group of dementias characterised by progressive degeneration of the frontal and temporal lobes. Typically presents with personality change, disinhibition, apathy, or language impairment rather than memory loss. Often affects younger adults (40s–60s).
- Acetylcholinesterase inhibitors
- Drugs (e.g., donepezil, rivastigmine, galantamine) that prevent breakdown of acetylcholine, increasing its availability. Used symptomatically in mild-to-moderate Alzheimer's disease and DLB. Produce modest improvements in cognition and function but do not halt disease progression.