Open AccessPINK1 Activation Attenuates Impaired Neuronal-Like Differentiation and Synaptogenesis and Mitochondrial Dysfunction in Alzheimer’s Disease Trans-Mitochondrial Cybrid Cells
Author(s) -
Fang Du,
Qinghua Yu,
Shirley ShiDu Yan
Publication year - 2021
Publication title -
journal of alzheimer's disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.677
H-Index - 139
eISSN - 1875-8908
pISSN - 1387-2877
DOI - 10.3233/jad-210095
Subject(s) - pink1 , mitochondrion , mitophagy , microbiology and biotechnology , biology , mitochondrial fusion , autophagy , synaptogenesis , dnaja3 , apoptosis , mitochondrial dna , biochemistry , gene
Mitochondrial dysfunction, bioenergetic deficit, and extensive oxidative stress underlie neuronal perturbation during the early stage of Alzheimer's disease (AD). Previously, we demonstrated that decreased PTEN-induced putative kinase 1 (PINK1) expression is associated with AD pathology in AD-affected human brains and AD mice.