How brain cells react to injury
- Lesion
Neurons cannot divide, so they show injury by shrinking, swelling or storing debris; astrocytes and microglia answer with scars and clusters.
What it is
The brain has a small set of cellular reactions that the pathologist reads like a vocabulary. Neurons turn shrunken and pink when they die acutely, round up when their axon is cut, and collect inclusions in degenerative, viral and storage diseases. Astrocytes proliferate and make a glial scar instead of collagen, and microglia gather into nodules around dying neurons. Recognising these patterns tells the type and the age of an injury.
Structure
- Neurons: acute injury gives red neurons; chronic degeneration shows first as lost synapses, then neuron loss with reactive gliosis.
- Astrocytes: in gliosis the cell bodies enlarge and the cytoplasm turns pink (gemistocytes); long-standing scars are dense meshes of fine processes.
- Rosenthal fibres: thick, bright eosinophilic, corkscrew-shaped bodies in astrocyte processes of old gliosis and pilocytic astrocytoma.
- Corpora amylacea: round, layered, basophilic, PAS-positive bodies in astrocyte end-feet; more with age, no disease meaning.
- Alzheimer type II astrocytes: enlarged pale nuclei with marginated chromatin, typical of hyperammonemia (hepatic encephalopathy).
- Microglia: rod cells and nodules in infection; myelin-laden macrophages (foamy) clean up infarcts and demyelination.
- Ependyma: injury gives ependymal granulations, small bumps of glia under the lining, after ventriculitis such as CMV.
Cellular reactions and what they usually mean
| Finding | Cell | Points to |
|---|---|---|
| Red (eosinophilic) neuron | Neuron | Acute irreversible injury: hypoxia, ischemia, hypoglycemia |
| Central chromatolysis | Neuron | Axon damage with attempted regeneration |
| Neurofibrillary tangle, Lewy body | Neuron | Neurodegenerative proteinopathy |
| Negri, Cowdry, owl-eye inclusions | Neuron or glia | Rabies, herpes simplex or zoster, CMV |
| Gemistocytic gliosis | Astrocyte | Any injury: the brain's scar |
| Alzheimer type II astrocyte | Astrocyte | High ammonia (liver failure) |
| Microglial nodule, neuronophagia | Microglia | Viral encephalitis, rickettsia, HIV |
| Sheets of foamy macrophages | Microglia and blood macrophages | Resolving infarct, demyelination |
Markers
- GFAP (astrocytes)
- Iba1, CD68 (microglia, macrophages)
- Neurofilament, NeuN (neurons)
- Ubiquitin, p62 (inclusions)
- PAS (corpora amylacea)
Clinical notes
- Because mature neurons do not divide, even a small loss in a critical region gives a permanent deficit; recovery depends on surviving circuits.
- Groups of neurons that share metabolism or connections fail together (selective vulnerability), which is why diseases map to systems.
Test yourself
Think of the answer, then tap the question to see it.
How soon after an irreversible hypoxic injury do red neurons appear?
From about 6 to 12 hours: the cell shrinks, the nucleus is pyknotic and the cytoplasm becomes intensely eosinophilic.
What does the brain use instead of collagen to scar?
Reactive astrocytes: gliosis, a dense mesh of GFAP-positive glial processes.
Which astrocyte change suggests hepatic encephalopathy?
Alzheimer type II astrocytes, with enlarged pale nuclei, caused by high ammonia.
Elsewhere in DurgiPedia
- The neuron and synapse
- Glial cells: astrocytes, oligodendrocytes, microglia, Schwann cells
- Nerve injury and regeneration (Wallerian degeneration)
- Gray and white matter, cerebellar cortex, meninges
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Brain Diseases | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.