Behavioral and neuropathologic changes induced by central injection of carboxyl-terminal fragment of beta-amyloid precursor protein in mice.

Abstract:

:Expression of the carboxyl-terminal fragment (CT) of the beta-amyloid precursor protein (APP) in transgenic animals has been linked with neurotoxicity. However, it remains to be clarified whether the neurotoxicity is caused by beta-amyloid proteins (A betas) derived from CT or by CT itself. To study the in vivo neurotoxicity of CT, mice were given a single intracerebroventricular injection of a recombinant 105-amino acid CT (CT105; 68.5-685 pmol, intracerebroventricularly), and changes in behavior and in brain histology were examined. Animals given CT105 (410 or 685 pmol, intracerebroventricularly) showed a dose-dependent impairment in the passive avoidance performance, whereas boiled CT105 had no effect. CT105 (685 pmol, intracerebroventricularly) induced reactive gliosis in neocortex and hippocampus and neurodegeneration in neocortex. These results indicate that centrally administered CT105 induces behavioral impairment and neuropathologic changes, suggesting a direct toxic effect of CT105 per se.

journal_name

J Neurochem

authors

Song DK,Won MH,Jung JS,Lee JC,Kang TC,Suh HW,Huh SO,Paek SH,Kim YH,Kim SH,Suh YH

doi

10.1046/j.1471-4159.1998.71020875.x

subject

Has Abstract

pub_date

1998-08-01 00:00:00

pages

875-8

issue

2

eissn

0022-3042

issn

1471-4159

journal_volume

71

pub_type

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