Amyloid precursor protein accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat

• Published in: Brain research Vol. 593; no. 1; p. 128
• Main Authors: Stephenson, D T, Rash, K, Clemens, J A
• Format: Journal Article
• Language: English
• Published: Netherlands 09.10.1992
• Subjects: Amyloid beta-Protein Precursor - metabolism; Animals; Axons - metabolism; Axons - ultrastructure; Brain - metabolism; Brain - pathology; Cerebral Arteries; Cerebral Infarction - metabolism; Cerebral Infarction - pathology; Immunohistochemistry; Ischemic Attack, Transient - metabolism; Ischemic Attack, Transient - pathology; Male; Nerve Degeneration; Neurites - metabolism; Neurites - ultrastructure; Neurons - metabolism; Neurons - pathology; Rats; Rats, Inbred SHR
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(92)91274-I

The distribution of beta-amyloid precursor protein (APP) was examined immunocytochemically in rats subjected to focal cerebral ischemia by permanent occlusion of the middle cerebral artery. At 4 and 7 days post-occlusion, APP immunoreactivity was preferentially localized within axonal swellings, dystrophic neurites and neuronal perikarya all along the periphery of the infarct. Immunolabeling was observed with antibodies generated against N-terminal, midregion, and C-terminal domains of APP. No immunoreactivity was observed with antisera directed against beta-amyloid protein (beta A4) itself. This pathological accumulation of APP is consistent with alterations of APP recently described in other models of neurodegeneration and implies a role for this protein in the response to CNS injury.