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.
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