Neurocognitive Disorders

Neurocognitive disorders encompass a group of conditions in which cognitive functioning is significantly impaired compared to a prior level of performance. They range from the relatively subtle deficits of Mild Neurocognitive Disorder to the profound loss of independence seen in Major Neurocognitive Disorder — what was previously called dementia.

01

Progressive

Neurocognitive disorders worsen over time. Unlike delirium, they are not acute or self-resolving.

02
Prior level
Current

Compared to prior level

Diagnosis requires a measurable decline from the individual's own previous baseline — not a comparison to population norms.

Mild, Major & Delirium.

The DSM-5 organises neurocognitive conditions across a spectrum of severity. Delirium stands apart — it is acute, fluctuating, and often reversible.

MiNDMild

Mild Neurocognitive Disorder

Modest cognitive decline from a prior level that does not interfere significantly with daily independence. Replaces the older term "mild cognitive impairment." Around 10–15% of cases progress to MaND per year.

Daily independence preserved
MaNDMajor

Major Neurocognitive Disorder

Significant cognitive decline in one or more domains (memory, executive function, language, etc.) that interferes with independence in everyday activities. The DSM-5 replacement for "dementia."

Independence significantly affected
DELAcute

Delirium

An acute, fluctuating disturbance of attention and awareness caused by an underlying medical condition, substance intoxication or withdrawal, or medication. Distinguished from dementia by its sudden onset and fluctuating course.

Acute onset · Often reversible

The major neurocognitive disorders.

Each disorder has a distinct profile of onset, pathology, and affected brain regions. Click a card to expand details.

AD

Gradual episodic memory loss

VaD

Stepwise decline

LBD

REM sleep behaviour disorder

FTD

Personality change

PD

Motor symptoms

Arnold Pick

1851–1924

Czech neurologist who described cases of progressive dementia associated with focal atrophy of the frontal and temporal lobes — now known as frontotemporal dementia, or "Pick's disease" in its classical form. His work established that different anatomical patterns of neurodegeneration could produce distinct clinical syndromes.

Emil Kraepelin

1856–1926

German psychiatrist who coined the term "Alzheimer's disease" in the 1910 edition of his psychiatry textbook, bringing Alzheimer's case descriptions to wide clinical attention. Kraepelin's systematic approach to classifying psychiatric disorders laid the groundwork for modern diagnostic systems.

Alois Alzheimer

1864–1915

German psychiatrist and neuropathologist who in 1906 described the first documented case of the disease that bears his name — a 51-year-old woman (Auguste Deter) with progressive memory loss, language problems, and behavioural changes. Post-mortem examination revealed the plaques and tangles now recognised as hallmarks of Alzheimer's disease.

Friedrich Heinrich Lewy

1885–1950

German-American neurologist who discovered the intracellular protein inclusions (Lewy bodies) found in Parkinson's disease while working in Alois Alzheimer's laboratory in 1912. Lewy bodies were later found to be the defining pathology of Dementia with Lewy Bodies, a major dementia subtype.

Major Neurocognitive Disorder (MaND)

The DSM-5 term replacing "dementia." Involves significant cognitive decline from a prior level in one or more domains (memory, executive function, language, etc.) that interferes with independence in everyday activities.

Mild Neurocognitive Disorder (MiND)

Modest cognitive decline that does not interfere significantly with daily independence. Replaces the term "mild cognitive impairment." Approximately 10–15% of cases progress to MaND per year, but many remain stable or revert to normal.

Delirium

An acute, fluctuating disturbance of attention and awareness caused by an underlying medical condition, substance intoxication/withdrawal, or medication. Distinguished from dementia by its acute onset and fluctuating course. Common in hospitalised older adults.

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 the clinical triad of fluctuating cognition, visual hallucinations, and Parkinsonism.

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.

Last reviewed July 2025
  1. 1.

    American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). APA Publishing.

    +About this source

    Diagnostic criteria and classification framework for major and mild neurocognitive disorders.

  2. 2.

    Petersen R.C., Smith G.E., Waring S.C., Ivnik R.J., Tangalos E.G., & Kokmen E. (1999). Mild cognitive impairment: clinical characterization and outcome. Archives of Neurology, 56(3), 303–308.

    +About this source

    Foundational paper defining mild cognitive impairment as a transitional state between normal ageing and dementia.

  3. 3.

    Prince M., Wimo A., Guerchet M., Ali G.-C., Wu Y.-T., & Prina M. (2015). World Alzheimer Report 2015: The Global Impact of Dementia. Alzheimer's Disease International.

    +About this source

    Comprehensive global epidemiology of dementia, informing prevalence figures and burden estimates.