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Early Disruption of Synaptic Function, Impairment of Plasticity, and Decreased of Cortical Circuit Connectivity in an Alzheimer’S Mouse Model of Amyloid Deposition

2021-11-04

Abstract excerpt

<title>Abstract</title> <p>Mutations in genes encoding amyloid precursor proteins and presenilins lead to increased β-amyloid (Aβ) production and cause familial Alzheimer’s disease (AD), a neurodegenerative disorder often associates with aging and features synapse loss and impaired synaptic plasticity. Aβ deposition is a pathological hallmark of AD. It is currently unknown whether and how AD risk alleles affects...

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Literature Corpus work
7cb704db-e510-5b19-bc37-45f787364150
DOI
10.21203/rs.3.rs-948437/v1
Open publication

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Early Disruption of Synaptic Function, Impairment of Plasticity, and Decreased of Cortical Circuit Connectivity in an Alzheimer’S Mouse Model of Amyloid DepositionDOI 10.21203/rs.3.rs-948437/v1
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