Abstract |
The beta-amyloid peptide-(25-35) fragment, but not beta-amyloid peptide-(1-28), shares with beta-amyloid protein-(1-42) the ability to self-aggregate and to induce neurotoxicity in vitro. This study examined the induction of amnesia in rats given intracerebroventricularly soluble or aggregated beta-amyloid peptide-(25-35) (5-45 nmol), or beta-amyloid peptide-(1-28) (15 nmol). Memory deficit in the water-maze test, examined 14 days after aggregated beta-amyloid peptide-(25-35) injection, was more pronounced than with soluble beta-amyloid peptide-(25-35). beta-Amyloid peptide-(1-28) only affected retention. These results confirm the direct amnesic properties of beta-amyloid peptides in the rat brain and showed that prior peptide aggregation markedly facilitates the appearance of amnesia.
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Authors | S Delobette, A Privat, T Maurice |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 319
Issue 1
Pg. 1-4
(Jan 14 1997)
ISSN: 0014-2999 [Print] Netherlands |
PMID | 9030890
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amyloid beta-Peptides
- Peptide Fragments
- amyloid beta-protein (25-35)
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Topics |
- Amnesia
(chemically induced)
- Amyloid beta-Peptides
(chemistry, toxicity)
- Animals
- Injections, Intraventricular
- Male
- Maze Learning
(drug effects)
- Peptide Fragments
(chemistry, toxicity)
- Rats
- Rats, Wistar
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