Publication Date:
2016-05-08
Description:
Article F1FO ATP synthase is a critical enzyme for the maintenance of mitochondrial function. Here the authors demonstrate that loss of the F1FO-ATP synthase subunit OSCP and the interaction of OSCP with Aβ peptide in Alzheimer’s disease patients and mouse models lead to F1FO-ATP synthase deregulation and disruption of synaptic mitochondrial function. Nature Communications doi: 10.1038/ncomms11483 Authors: Simon J. Beck, Lan Guo, Aarron Phensy, Jing Tian, Lu Wang, Neha Tandon, Esha Gauba, Lin Lu, Juan M. Pascual, Sven Kroener, Heng Du
Electronic ISSN:
2041-1723
Topics:
Biology
,
Chemistry and Pharmacology
,
Natural Sciences in General
,
Physics
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