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Early association of reactive astrocytes with senile plaques in Alzheimer's disease

Pike, Christian J., Cummings, Brian J., Cotman, Carl W.·1995·Experimental Neurology
DOI 10.1016/0014-4886(95)90022-5
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Abstract

The fibrillar beta-amyloid protein (A beta) plaques of Alzheimer's disease (AD) are associated with reactive astrocytes and dystrophic neurites and have been suggested to contribute to neurodegenerative events in the disease. We recently reported parallel in vitro and in situ findings, suggesting that the adoption of a reactive phenotype and the colocalization of astrocytes with plaques in AD may be mediated in large part by aggregated A beta. Thus, A beta-mediated effects on astrocytes may directly affect disease progression by modifying the degenerative plaque environment. Alternatively, plaque-associated reactive astrocytosis may primarily represent a glial response to the neural injury associated with plaques and not significantly contribute to AD pathology. To investigate the validity of these two positions, we examined the differential colocalization of reactive astrocytes and dystrophic neurites with plaques. Hippocampal sections from AD brains--ranging in neuropathology from mild to severe--were triple-labeled with antibodies recognizing A beta protein, reactive astrocytes, and dystrophic neurites. We observed not only plaques containing both or neither cell type, but also plaques containing (1) reactive astrocytes but not dystrophic neurites and (2) dystrophic neurites but not reactive astrocytes. The relative proportion of plaques colocalized with reactive astrocytes in the absence of dystrophic neurites is relatively high in mild AD but significantly decreases over…

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  • Upregulated ECM caused by astrogliosis is associated with amyloid plaques in AD and glial scar formation after CNS injury, creating a mechanical barrier for neurite outgrowth.

    “Upregulated ECM caused by astrogliosis is associated with amyloid plaques in AD and glial scar formation after CNS injury, creating a mechanical barrier for neurite outgrowth (Bovolenta et al., 1997; Pike et al., 1995).”

    From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Pike et al., 1995

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Metadata

Authors
Pike, C. J., Cummings, B. J., & Cotman, C. W.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
1995-04
Volume
132
Issue
2
Pages
172-179
ISSN
0014-4886
DOI
10.1016/0014-4886(95)90022-5
Cited by
164
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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