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A failure of β-amyloid physiological function due to genetic deletion of α7 nicotinic acetylcholine receptors induces an Alzheimer’s disease-like pathology

2021-01-07

Abstract excerpt

<h4>ABSTRACT</h4> The accumulation of amyloid-beta peptide (Aβ) and the failure of cholinergic transmission are key players in Alzheimer’s disease (AD). However, in the healthy brain, Aβ contributes to synaptic plasticity and memory acting through α7 subtype nicotinic acetylcholine receptors (α7nAChRs). Here, we hypothesized that the α7nAChR deletion blocks Aβ physiological function and promotes a compensatory in...

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Literature Corpus work
1778d94b-a029-5fe8-ac70-aa0c5e8dc22b
DOI
10.1101/2021.01.05.425382
Open publication

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A failure of β-amyloid physiological function due to genetic deletion of α7 nicotinic acetylcholine receptors induces an Alzheimer’s disease-like pathologyDOI 10.1101/2021.01.05.425382
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