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The intracerebral injection of Aβ1-42 oligomers does not invariably alter seizure susceptibility in mice.


ABSTRACT:

Objectives

Epileptiform activity and seizures are present in patients with Alzheimer's disease (AD) and genetic animal models of AD. Amyloid beta 1-42 (Aβ1-42) oligomers are thought to be crucial in AD and can cause neuronal hyperexcitability in vitro. However, it is unclear whether these Aβ1-42 oligomers cause the increased seizure susceptibility in vivo in people with AD and in AD animal models, nor via which mechanisms it would do so. We investigated this question by injecting Aβ1-42 oligomers intracerebrally in mice and assessed its impact on seizure susceptibility.

Materials and methods

We performed a single intracerebral injection of synthetic Aβ1-42 oligomers or scrambled Aβ1-42 in NMRI mice in three

SUBMITTER: Vande Vyver M 

PROVIDER: S-EPMC10512828 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature