Short communication
In vitro aggregation facilitates β-amyloid peptide-(25–35)-induced amnesia in the rat

https://doi.org/10.1016/S0014-2999(96)00922-3Get rights and content

Abstract

The β-amyloid peptide-(25–35) fragment, but not β-amyloid peptide-(1–28), shares with β-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 β-amyloid peptide-(25–35) (5–45 nmol), or β-amyloid peptide-(1–28) (15 nmol). Memory deficit in the water-maze test, examined 14 days after aggregated β-amyloid peptide-(25–35) injection, was more pronounced than with soluble β-amyloid peptide-(25–35). β-Amyloid peptide-(1–28) only affected retention. These results confirm the direct amnesic properties of β-amyloid peptides in the rat brain and showed that prior peptide aggregation markedly facilitates the appearance of amnesia.

References (16)

There are more references available in the full text version of this article.

Cited by (0)

View full text