Journal
CURRENT TOPICS IN MEDICINAL CHEMISTRY
Volume 16, Issue 8, Pages 849-857Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1568026615666150827095102
Keywords
Alzheimer's disease; Bioenergetics; Damage associated molecular pattern; Inflammation; Mitochondria
Categories
Funding
- University of Kansas Alzheimer's Disease Center [P30AG035982]
- Frank and Evangeline Thompson Alzheimer's Treatment Program Fund
- Hugh and Betty Libby Foundation
- Greater Kansas City Automobile Dealers Association
- Gene and Marge Sweeney Chair
- University of Kansas Alzheimer's Disease Center Pilot program
- Landon Center for Aging
- Frontiers the Heartland Institute for Clinical and Translational Research
- Kansas IDeA Network of Biomedical Research Excellence
- KUMC Biomedical Research Training Program
- NATIONAL INSTITUTE ON AGING [P30AG035982] Funding Source: NIH RePORTER
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Mitochondrial dysfunction and neuroinflammation occur in Alzheimer's disease (AD). The causes of these pathologic lesions remain uncertain, but links between these phenomena are increasingly recognized. In this review, we discuss data that indicate mitochondria or mitochondrial components may contribute to neuroinflammation. While mitochondrial dysfunction could cause neuroinflammation, neuroinflammation could also cause mitochondrial dysfunction. However, based on the systemic nature of AD mitochondrial dysfunction as well as data from experiments we discuss, the former possibility is perhaps more likely. If correct, then manipulation of mitochondria, either directly or through manipulations of bioenergetic pathways, could prove effective in reducing metabolic dysfunction and neuroinflammation in AD patients. We also review some potential approaches through which such manipulations may be achieved.
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