Mitochondrial abnormalities in Parkinson's disease and Alzheimer's disease: can mitochondria be targeted therapeutically?

Mitochondrial abnormalities have been identified as a central mechanism in multiple neurodegenerative diseases and, therefore, the mitochondria have been explored as a therapeutic target. This review will focus on the evidence for mitochondrial abnormalities in the two most common neurodegenerative...

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Vydáno v:Biochemical Society transactions Ročník 46; číslo 4; s. 891
Hlavní autoři: Macdonald, Ruby, Barnes, Katy, Hastings, Christopher, Mortiboys, Heather
Médium: Journal Article
Jazyk:angličtina
Vydáno: England 20.08.2018
Témata:
Alzheimer Disease - drug therapy
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Animals
Antioxidants - metabolism
Antioxidants - pharmacology
Drug Delivery Systems
Humans
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondrial Dynamics
Mitochondrial Proteins - metabolism
Models, Biological
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Parkinson Disease - drug therapy
Parkinson Disease - metabolism
Parkinson Disease - pathology
therapeutics
mitochondrial dysfunction
Parkinson's disease
Alzheimer's disease
ISSN:1470-8752, 1470-8752
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Shrnutí:Mitochondrial abnormalities have been identified as a central mechanism in multiple neurodegenerative diseases and, therefore, the mitochondria have been explored as a therapeutic target. This review will focus on the evidence for mitochondrial abnormalities in the two most common neurodegenerative diseases, Parkinson's disease and Alzheimer's disease. In addition, we discuss the main strategies which have been explored in these diseases to target the mitochondria for therapeutic purposes, focusing on mitochondrially targeted antioxidants, peptides, modulators of mitochondrial dynamics and phenotypic screening outcomes.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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ISSN:1470-8752
1470-8752
DOI:10.1042/BST20170501