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Erschienen in: Medical Molecular Morphology 1/2019

23.04.2018 | Review

BRI2 as an anti-Alzheimer gene

verfasst von: Shuji Matsuda, Takao Senda

Erschienen in: Medical Molecular Morphology | Ausgabe 1/2019

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Abstract

There are several theories regarding the etiologies of Alzheimer disease (AD). Considering that all genes responsible for familial AD are amyloid protein precursor (APP) or APP metabolizing enzymes, surely aberrant APP metabolism is crucial to pathogenesis of AD. BRI2, a type II transmembrane protein, binds APP and inhibits all α, β, and γ pathways of APP proteolysis. Crossing AD model mice with BRI2 transgenic or BRI2 knockout mice confirmed that BRI2 is an anti-Alzheimer gene. Mutations of BRI2 are known to cause rare familial dementias in human. Analysis of knock-in mice harboring the disease mutation revealed the memory defect in the mice, attributable to loss of protective function of BRI2. Further studies are needed to decipher this anti-Alzheimer mechanism of BRI2 to develop a novel therapeutic application for AD. In this review, after describing basic assumptions in AD study, we focus on BRI2 as an anti-Alzheimer gene.
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Metadaten
Titel
BRI2 as an anti-Alzheimer gene
verfasst von
Shuji Matsuda
Takao Senda
Publikationsdatum
23.04.2018
Verlag
Springer Japan
Erschienen in
Medical Molecular Morphology / Ausgabe 1/2019
Print ISSN: 1860-1480
Elektronische ISSN: 1860-1499
DOI
https://doi.org/10.1007/s00795-018-0191-1

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