PubMed · 5938787
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E R Hilgard. 1966. Posthypnotic amnesia: experiments and theory.. https://doi.org/10.1080/00207146608412953
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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.
Severe transient postoperative memory deficits among epilepsy patients with resection from one temporal lobe may be indicative of increased risk for amnesia had more extensive removal of mesial structures occurred. Immediate postoperative testing may provide some validation for risk of amnesia as predicted by the intracarotid sodium amobarbital memory test (IAP-M). Thirty patients (24 not considered at risk for amnesia and 5 who failed the IAP-M) were tested on the first, second, and third days following resection from the right or left temporal lobe. Results suggest that the IAP-M paradigm used does not necessarily predict postoperative memory performance.