Mitochondrial therapeutic interventions in Alzheimer’s disease
Alzheimer's Disease (AD) is one of the most common age-related neurodegenerative diseases in the developed world. Treatment of AD is particularly challenging as the drug must overcome the blood brain barrier (BBB) before it can reach its target. Mitochondria are recognized as one of the most im...
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Published in | Journal of the neurological sciences Vol. 395; pp. 62 - 70 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
15.12.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Alzheimer's Disease (AD) is one of the most common age-related neurodegenerative diseases in the developed world. Treatment of AD is particularly challenging as the drug must overcome the blood brain barrier (BBB) before it can reach its target. Mitochondria are recognized as one of the most important targets for neurological drugs as the organelle is known to play a critical role in diverse cellular processes such as energy production and apoptosis regulation. Mitochondrial targeting was originally developed to study mitochondrial dysfunction and the organelles interaction with other sub-cellular organelles. The purpose of this review is to provide an overview of mitochondrial dysfunction and its role in late onset AD pathology. We then highlight recent antioxidant and enzymatic treatments used to alleviate mitochondrial dysfunction. Finally, we describe current applications of targeted mitochondrial delivery in the treatment of AD.
•Highlighted an overview of mitochondrial dysfunction and its role in late onset Alzheimer's Disease pathology.•Highlighted recent antioxidant and enzymatic treatments used to alleviate mitochondrial dysfunction.•Described current applications of targeted mitochondrial delivery in the treatment of AD. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0022-510X 1878-5883 |
DOI: | 10.1016/j.jns.2018.09.033 |