Is there a link between inorganic polyphosphate (polyP), mitochondria, and neurodegeneration?
Alzheimer’s disease
Inorganic polyphosphate
Mitochondria
Neurodegeneration
Parkinson’s disease
polyP
Journal
Pharmacological research
ISSN: 1096-1186
Titre abrégé: Pharmacol Res
Pays: Netherlands
ID NLM: 8907422
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
27
07
2020
revised:
08
09
2020
accepted:
15
09
2020
pubmed:
4
10
2020
medline:
18
11
2021
entrez:
3
10
2020
Statut:
ppublish
Résumé
Mitochondrial dysfunction - including increased apoptosis, calcium and protein dyshomeostasis within the organelle, and dysfunctional bioenergetics and oxidative status - is a common, early feature in all the major neurodegenerative diseases, including Alzheimer's Disease (AD) and Parkinson's Disease (PD). However, the exact molecular mechanisms that drive the organelle to dysfunction and ultimately to failure in these conditions are still not well described. Different authors have shown that inorganic polyphosphate (polyP), an ancient and well-conserved molecule, plays a key role in the regulation of mitochondrial physiology under basal conditions. PolyP, which is present in all studied organisms, is composed of chains of orthophosphates linked together by highly energetic phosphoanhydride bonds, similar to those found in ATP. This polymer shows a ubiquitous distribution, even if a high co-localization with mitochondria has been reported. It has been proposed that polyP might be an alternative to ATP for cellular energy storage in different organisms, as well as the implication of polyP in the regulation of many of the mitochondrial processes affected in AD and PD, including protein and calcium homeostasis. Here, we conduct a comprehensive review and discussion of the bibliography available regarding the role of polyP in the mitochondrial dysfunction present in AD and PD. Taking into account the data presented in this review, we postulate that polyP could be a valid, innovative and, plausible pharmacological target against mitochondrial dysfunction in AD and PD. However, further research should be conducted to better understand the exact role of polyP in neurodegeneration, as well as the metabolism of the polymer, and the effect of different lengths of polyP on cellular and mitochondrial physiology.
Identifiants
pubmed: 33010423
pii: S1043-6618(20)31519-X
doi: 10.1016/j.phrs.2020.105211
pmc: PMC7855267
mid: NIHMS1633842
pii:
doi:
Substances chimiques
Amyloid
0
Polyphosphates
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
105211Subventions
Organisme : NIA NIH HHS
ID : R00 AG055701
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
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