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Neurotoxicity and Oxidative Damage of Beta Amyloid 1–42 versus Beta Amyloid 1–40 in the Mouse Cerebral Cortex
Author(s) -
KLEIN AUTUMN M.,
KOWALL NEIL W.,
FERRANTE ROBERT J.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07845.x
Subject(s) - beta (programming language) , senile plaques , neurotoxicity , amyloid beta , glial fibrillary acidic protein , chemistry , amyloid (mycology) , cerebral cortex , pathology , cortex (anatomy) , oxidative stress , alzheimer's disease , immunohistochemistry , endocrinology , biology , biochemistry , medicine , toxicity , neuroscience , disease , peptide , organic chemistry , computer science , programming language
Senile plaques (SP), a neuropathological hallmark of Alzheimer's disease (AD), are characterized by extracellular accumulations of beta amyloid (A beta). SP predominantly contain A beta 42 with a small amount of associated A beta 40. We determined the neurotoxic properties of A beta 42 as compared to A beta 40 by injections into the frontal cortex of three month old C57BL/6 mice. A beta 42 was associated with a significantly larger area of glial fibrillary acidic protein (GFAP) immunoreactivity and a greater density of reactive astrocytes than A beta 40. Immunohistochemical staining for markers of oxidative damage against 3-nitrotyrosine (3-NT) and 8-hydroxydeoxyguanosine (8-OHDG) were significantly more intense around the A beta 42 injection compared to the A beta 40 injection sites. These findings are consistent with previous in vitro studies and suggest that A beta 42 is more neurotoxic and may generate more free radical damage than A beta 40.