Abnormal interaction of Rlip with mutant APP/Abeta and phosphorylated tau reduces wild-type Rlip levels and disrupt Rlip function in Alzheimer's disease
- PMID: 37633469
- DOI: 10.1016/j.bbadis.2023.166858
Abnormal interaction of Rlip with mutant APP/Abeta and phosphorylated tau reduces wild-type Rlip levels and disrupt Rlip function in Alzheimer's disease
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease that affects a large proportion of the aging population. RalBP1 (Rlip) is a stress-activated protein, that plays an important role in aging and neurodegenerative diseases such as Alzheimer's disease. Mutant APP and mutant Tau interact with the Rlip protein which leads to decreased wild-type Rlip levels and disrupt Rlip function in Alzheimer's disease. Rlip is a promising new target for aging, Alzheimer's disease, and other neurological diseases.
Keywords: Alzheimer's disease; Mitochondrial dysfunction; Oxidative stress; Rlip protein.
Copyright © 2023 Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare that a pending disclosure is in progress with the contents of this study.
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