Co-injection of beta-amyloid with ibotenic acid induces synergistic loss of rat hippocampal neurons
Abstract
Senile plaques are a pathological hallmark of Alzheimer's disease. The major component of senile plaques is beta-amyloid which consists of approximately 4000 mol. wt of peptide. Accumulating evidence suggests that beta-amyloid may represent the underlying cause of Alzheimer's disease. In vitro, beta-amyloid has been shown either to be directly neurotoxic or to potentiate neurotoxic effects of excitatory amino acids. However, beta-amyloid toxicity in vivo has not always been reproducible. In this study, we injected beta-amyloid fragment 1-40 or 25-35 alone or in combination with a small amount of ibotenic acid, an excitatory amino acid, into rat hippocampus, and examined the histological and immunohistochemical changes two weeks after injection. Although beta-amyloid alone or ibotenic acid alone exerted only minimal degenerating effects on neurons just around the injection site, the co-injection of beta-amyloid 1-40 or beta-amyloid 25-35 with ibotenic acid produced drastic neuronal loss; the haematoxylin-eosin staining revealed that most neurons not only around the injection site but also in distant areas including CA1, CA4 and dentate gyrus were depleted. The neuronal loss occurred in a dose-dependent manner with respect to ibo...Continue Reading
References
Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein
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