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Neuropathology — neurodegenerative disease, herpes encephalitis, Wernicke and amyloid angiopathy
Neurodegenerative brain diseases are defined pathologically by the protein that accumulates — Aβ and tau in Alzheimer disease, α-synuclein in Parkinson disease and Lewy body disease, TDP-43 in ALS and some frontotemporal dementias, and prion protein in Creutzfeldt-Jakob disease — and alongside them it is important to know conditions that mimic them: herpes encephalitis, Wernicke encephalopathy and haemorrhage from amyloid angiopathy.
Why it matters in the exam
The bank asks about stains, sites and defined findings. In Alzheimer disease there are neuritic plaques with an Aβ core and neurofibrillary tangles of phosphorylated tau, well seen with silver stains or immunohistochemistry; changes begin in the entorhinal area and hippocampus and spread to the cortex (Braak stages). In Parkinson disease there is loss of pigmented neurons in the substantia nigra and Lewy bodies of α-synuclein; when Lewy bodies are scattered in the cortex with early dementia and hallucinations — Lewy body disease. In Huntington disease there is atrophy of the caudate nucleus.
HSV-1 encephalitis in a person without immunosuppression presents with behavioural change and acute memory impairment, and affects the temporal lobes and inferior frontal region with haemorrhagic necrosis, with nuclear inclusion bodies. Wernicke encephalopathy results from thiamine deficiency, mainly in people with alcohol use disorder and malnutrition, and affects the mammillary bodies and the area around the third ventricle; in the chronic form (Korsakoff) there is impaired short-term memory and confabulation. Amyloid angiopathy — Aβ in the walls of small cortical vessels — causes recurrent lobar haemorrhages in older adults, different from the sites of hypertensive haemorrhage (basal ganglia, thalamus, pons).
In Creutzfeldt-Jakob disease there is spongiform change (vacuoles in the neuropil), neuronal loss and gliosis without inflammation, and the protein is misfolded prion protein; a special decontamination procedure is needed at autopsy and in the laboratory. In ALS there is loss of upper and lower motor neurons and TDP-43 inclusions. An autopsy rule: a fresh brain not fixed in formalin is hard to examine, so the whole brain is usually fixed before cutting, unless fresh samples are needed for culture or molecular tests.
Key points
- Alzheimer: Aβ and tau, beginning in the entorhinal area and hippocampus.
- Parkinson: substantia nigra and α-synuclein.
- HSV-1: haemorrhagic necrosis of the temporal lobes.
- Wernicke and Korsakoff: thiamine, mammillary bodies, short-term memory.
- Amyloid angiopathy: lobar haemorrhages in older adults.
Summary table
| Disease | Protein or cause | Site | Key finding |
|---|---|---|---|
| Alzheimer | Aβ and tau | Entorhinal, hippocampus, cortex | Plaques and tangles; silver stain |
| Parkinson and Lewy body disease | α-synuclein | Substantia nigra; cortex in Lewy body disease | Loss of pigmented neurons, Lewy bodies |
| HSV-1 encephalitis | HSV-1 | Temporal lobes, inferior frontal | Haemorrhagic necrosis |
| Wernicke and Korsakoff | Thiamine deficiency | Mammillary bodies, around the third ventricle | Short-term memory loss, confabulation |
| Amyloid angiopathy | Aβ in vessels | Cortex | Lobar haemorrhages in older adults |
In the full version for subscribers
- A simple algorithm
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Sources
- Greenfield's Neuropathology, 9th edition (2018) — Neurodegenerative diseases; viral infections; nutritional disorders
- NIA-AA guidelines for the neuropathologic assessment of Alzheimer disease, 2012 — ABC score
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — The central nervous system
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.