ArticleScientific reports2025
Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of alzheimer's disease.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- [Noninvasive nanosecond transcranial pulsed electric fields: deep-penetrating, high-field stimulation for suppressing hippocampal amyloid-β and improving cognitive function in an Alzheimer's disease model].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026Article
- Exercise-induced GPLD1 is associated with neuroprotection and improvement of hippocampal dysfunction in an Alzheimer's disease model.Metabolic brain disease · 2026Article
- Nano-magnolol enhances the modulatory effects of magnolol on cognitive performance and BACE1-related biochemical changes in an STZ-induced rat model of Alzheimer's disease.Discover nano · 2026Article
- Amyloid-Frontiers in aging neuroscience · 2026Article
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Abstract
Current therapeutic strategies for Alzheimer's disease (AD) target amyloid-beta (Aβ) fibrils and high molecular weight protofibrils associated with plaques, but molecular cascades associated with AD may drive neural systems failure before Aβ plaque deposition in AD. Employing hippocampal electrophysiological recordings and dynamic calcium imaging across the sleep-wake cycle in a freely behaving mouse model of AD before Aβ plaques accumulated, we detected marked impairments of hippocampal systems function: In a spatial behavioral task, phase-amplitude coupling (PAC) of the hippocampal theta and gamma oscillations was impaired and place cell calcium fluctuations were hyper-synchronized with the theta oscillation. These changes were not observed in REM sleep. In subsequent slow wave sleep (SWS), place cell reactivation was reduced. These degraded neural functions underlying memory encoding and consolidation support targeting pathological processes of the pre-plaque phase of AD to treat and prevent hippocampal impairments.
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