Co-localization of apolipoprotein E and beta-amyloid in plaques and cerebral blood vessels of aged non-human primates

Citation
Jb. Summers et al., Co-localization of apolipoprotein E and beta-amyloid in plaques and cerebral blood vessels of aged non-human primates, ALZHEIM REP, 1(2), 1998, pp. 119-128
Citations number
39
Categorie Soggetti
Neurology
Journal title
ALZHEIMERS REPORTS
ISSN journal
14616130 → ACNP
Volume
1
Issue
2
Year of publication
1998
Pages
119 - 128
Database
ISI
SICI code
1461-6130(199803)1:2<119:COAEAB>2.0.ZU;2-6
Abstract
The regional, structural and cellular localization of apolipoprotein E (apo E) was examined in the brains of 15 non-human primates. The presence of bot h apoE and beta-amytoid (A beta) in tissue sections was visualized by dual- label fluorescent immunohistochemistry. Additionally, dual label studies of glial fibrillary acidic protein (GFAP) and A beta were used to investigate the orientation of astrocytes to plaques, and apoE and GFAP dual labeling was used to determine whether astrocytes or other brain cells in monkeys we re potential sources for brain apoE. ApoE immunoreactivity (IR) was associa ted with all plaques and cerebrovascular amyloid in five aged moneys. GFAP immunoreactive astrocytes were also observed in the neuropil surrounding so me plaques, but apoE IR was not observed in the cell bodies of astrocytes i n these five monkeys. These results support an early role for apoE in the d evelopment of plaques and cerebrovascular amyloid in the brains of non-huma n primates. Furthermore, the inability to detect apoE IR in the cell bodies of astrocytes in these monkeys does not support the hypothesis that. plaqu e or blood vessel associated apoE is principally derived from astrocytes, h owever apoE labeling of certain neurons was readily observed. Additionally, we report that the basal ganglia of rhesus and long tailed macaques, simil ar to human basal ganglia, are targets for plaque formation. These findings also emphasize the value of nonhuman primates for investigating mechanisms of human neurodegenerative disorders, including Alzheimer's disease.