Presenilin Deficiency Increases Susceptibility to Oxidative Damage in Fibroblasts.

Alzheimer’s disease ferritin iron oxidative presenilin

Journal

Frontiers in aging neuroscience
ISSN: 1663-4365
Titre abrégé: Front Aging Neurosci
Pays: Switzerland
ID NLM: 101525824

Informations de publication

Date de publication:
2022
Historique:
received: 23 03 2022
accepted: 27 05 2022
entrez: 5 7 2022
pubmed: 6 7 2022
medline: 6 7 2022
Statut: epublish

Résumé

Alzheimer's disease (AD) is a genetic and sporadic neurodegenerative disease characterized by extracellular amyloid-β-protein (Aβ) aggregates as amyloid plaques and neuronal loss in the brain parenchyma of patients. Familial AD (FAD) is found to be genetically linked to missense mutations either in presenilin (PS) or amyloid precursor protein (APP). Most of PS mutations increase Aβ42/Aβ40 ratio, which is thought to result in early amyloid deposition in brain. However, PS deficiency in the fore brain of adult mouse leads to neuronal loss in an Aβ independent manner and the underlying mechanism is largely unknown. In this study, we found that reactive oxygen species (ROS) are increased in PS deficient fibroblasts and that H

Identifiants

pubmed: 35783133
doi: 10.3389/fnagi.2022.902525
pmc: PMC9243443
doi:

Types de publication

Journal Article

Langues

eng

Pagination

902525

Informations de copyright

Copyright © 2022 Zou, Islam, Sun, Gao, Nakamura, Komano, Tomita and Michikawa.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Kun Zou (K)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Sadequl Islam (S)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Yang Sun (Y)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Yuan Gao (Y)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Tomohisa Nakamura (T)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Hiroto Komano (H)

Advanced Prevention and Research Laboratory for Dementia, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.

Taisuke Tomita (T)

Laboratory of Neuropathology and Neuroscience, Faculty of Pharmaceutical Sciences, University of Tokyo, Bunkyo City, Japan.

Makoto Michikawa (M)

Department of Biochemistry, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

Classifications MeSH