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Mitochondria and Alzheimer's disease: amyloid-beta peptide uptake and degradation by the presequence protease, hPreP
Stockholm University, Faculty of Science, Department of Biochemistry and Biophysics.
Stockholm University, Faculty of Science, Department of Biochemistry and Biophysics.
2009 (English)In: Journal of Bioenergetics and Biomembranes, ISSN 0145-479X, E-ISSN 1573-6881, Vol. 41, no 5, 447-451 p.Article in journal (Refereed) Published
Abstract [en]

Several lines of evidence suggest mitochondrial dysfunction as a possible underlying mechanism of Alzheimer's disease (AD). Accumulation of the amyloid-beta peptide (Abeta), a neurotoxic peptide implicated in the pathogenesis of AD, has been detected in brain mitochondria of AD patients and AD transgenic mouse models. In vitro evidence suggests that the Abeta causes mitochondrial dysfunction e.g. oxidative stress, mitochondrial fragmentation and decreased activity of cytochrome c oxidase and TCA cycle enzymes. Here we review the link between mitochondrial dysfunctions and AD. In particular we focus on the mechanism for Abeta uptake by mitochondria and on the recently identified Abeta degrading protease in human brain mitochondria.

Place, publisher, year, edition, pages
2009. Vol. 41, no 5, 447-451 p.
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Biochemistry and Molecular Biology
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URN: urn:nbn:se:su:diva-34993DOI: 10.1007/s10863-009-9244-4ISI: 000271421900008PubMedID: 19798557OAI: oai:DiVA.org:su-34993DiVA: diva2:286069
Available from: 2010-01-13 Created: 2010-01-13 Last updated: 2017-02-22Bibliographically approved

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Alikhani, NyoshaGlaser, Elzbieta
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