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Immunohistochemical study of apolipoprotein E in human cerebrovascular white matter lesions
H Tomimoto1, I Akiguchi, T Suenaga
1Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Abstract:
In the brains of ine cases with cerebrovascular disease, one with mixed dementia, one with amyloid angiopathy and two non-neurological controls, we found three cases with focal accumulation of apolipoprotein E (apo-E) in dystrophic axons and accompanying macrophages. Since amyloid precursor protein (APP) and chromogranin A (CgA) accumulate after axonal damages, and are sensitive markers of the white matter lesions, the regional distribution of apo-E was compared to that of APP and CgA. apo-E-immunoreactive axons were present in the periphery of an infarction with neighboring macrophages, but not in mild white matter lesions that contained APP- or CgA-immunoreactive fiber bundles. The results suggest a role of apo-E in recycling cholesterol and other membrane components via macrophages into remodeling neurites in the brain, but this phenomenon is restricted to the periphery of infarction and may be less prominent than in the peripheral nervous system.
Insights
Apolipoprotein E (apo-E) accumulates in damaged brain axons near infarcts, suggesting a role in cholesterol recycling via macrophages. This process appears distinct from white matter lesions marked by amyloid precursor protein (APP) and chromogranin A (CgA).
Area of Science:
- Neuroscience
- Neuropathology
- Biochemistry
Background:
- Cerebrovascular disease and dementia are associated with complex neuropathological changes.
- Apolipoprotein E (apo-E) is implicated in lipid transport and neuronal repair.
- Amyloid precursor protein (APP) and chromogranin A (CgA) are markers of axonal damage and white matter lesions.
Purpose of the Study:
- To investigate the focal accumulation of apolipoprotein E (apo-E) in brain tissue from patients with cerebrovascular disease.
- To compare the regional distribution of apo-E with markers of axonal damage, APP and CgA.
Main Methods:
- Immunohistochemical analysis of brain tissue from patients with cerebrovascular disease (including mixed dementia and amyloid angiopathy) and non-neurological controls.
- Detection and localization of apo-E, APP, and CgA.
Main Results:
- Focal accumulation of apo-E was observed in dystrophic axons and macrophages in three cases.
- apo-E-immunoreactive axons were found at the periphery of infarcts, associated with macrophages.
- Mild white matter lesions containing APP or CgA did not show apo-E immunoreactivity.
Conclusions:
- Apolipoprotein E (apo-E) may play a role in recycling cholesterol and membrane components via macrophages into remodeling neurites.
- This apo-E-mediated process appears localized to the periphery of brain infarction.
- The mechanism seems less prominent in the central nervous system compared to the peripheral nervous system.