Arsenic and Tau Phosphorylation: a Mechanistic Review.
Arsenic
GSK-3
Hyperphosphorylation
Tau protein
Journal
Biological trace element research
ISSN: 1559-0720
Titre abrégé: Biol Trace Elem Res
Pays: United States
ID NLM: 7911509
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
received:
05
01
2023
accepted:
14
03
2023
medline:
2
11
2023
pubmed:
22
5
2023
entrez:
21
5
2023
Statut:
ppublish
Résumé
Arsenic poisoning can affect the peripheral nervous system and cause peripheral neuropathy. Despite different studies on the mechanism of intoxication, the complete process is not explained yet, which can prevent further intoxication and produce effective treatment. In the following paper, we would like to consider the idea that arsenic might cause some diseases via inflammation induction, and tauopathy in neurons. Tau protein, one of the microtubule-associated proteins expressed in neurons, contributes to neuronal microtubules structure. Arsenic may be involved in cellular cascades involved in modulating tau function or hyperphosphorylation of tau protein, which ultimately leads to nerve destruction. For proof of this assumption, some investigations have been planned to measure the association between arsenic and quantities of phosphorylation of tau protein. Additionally, some researchers have investigated the association between microtubule trafficking in neurons and the levels of tau protein phosphorylation. It should be noticed that changing tau phosphorylation in arsenic toxicity may add a new feature to understanding the mechanism of poisonousness and aid in discovering novel therapeutic candidates such as tau phosphorylation inhibitors for drug development.
Identifiants
pubmed: 37211576
doi: 10.1007/s12011-023-03634-y
pii: 10.1007/s12011-023-03634-y
doi:
Substances chimiques
tau Proteins
0
Arsenic
N712M78A8G
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
5708-5720Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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