Apolipoprotein J in Alzheimer's Disease: Shedding Light on Its Role with Cell Signaling Pathway Perspective and Possible Therapeutic Approaches.
Alzheimer’s disease
ApoJ
amyloid-beta
cell signaling pathway
clusterin
neurodegenerative disorders
Journal
ACS chemical neuroscience
ISSN: 1948-7193
Titre abrégé: ACS Chem Neurosci
Pays: United States
ID NLM: 101525337
Informations de publication
Date de publication:
16 12 2020
16 12 2020
Historique:
pubmed:
1
12
2020
medline:
22
6
2021
entrez:
30
11
2020
Statut:
ppublish
Résumé
Apolipoprotein J (ApoJ), or clusterin, is one of the main apolipoproteins in the brain. It is synthesized and released from astrocytes in a healthy brain, and its expression increases in neurodegenerative disorders. Genetic evidence has suggested an association between ApoJ polymorphism and the risk of Alzheimer's disease (AD)-it is now considered the third main genetic risk factor for late-onset AD. However, the role of ApoJ overexpression in the state of disorder, toxicity, or protection is not yet clear. Since ApoJ plays different roles in AD, we review the function of ApoJ using different cell signaling pathways in AD and outline its paradoxical roles in AD. ApoJ helps in amyloid-beta (Aβ) clearance. Vice versa, ApoJ gene knock-out causes fibrillary Aβ reduction and prevents Aβ-induced neuron cell death. Understanding ApoJ, through various cellular signaling pathways, creates a new perspective on AD's cellular principles. The overall message is that ApoJ can be a valuable tool in controlling AD.
Identifiants
pubmed: 33251792
doi: 10.1021/acschemneuro.0c00637
doi:
Substances chimiques
Amyloid beta-Peptides
0
Apolipoproteins E
0
Clusterin
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM