小柯机器人

美国西北大学Navdeep S. Chandel研究组利用脑线粒体复合体I功能障碍的小鼠模型发现，NAD+再生可挽救寿命，但不能挽救共济失调。2020年6月22日，《细胞—代谢》在线发表了这一成果。

Title: NAD+ Regeneration Rescues Lifespan, but Not Ataxia, in a Mouse Model of Brain Mitochondrial Complex I Dysfunction

Author: Gregory S. McElroy, Colleen R. Reczek, Paul A. Reyfman, Divakar S. Mithal, Craig M. Horbinski, Navdeep S. Chandel

Issue&Volume: 2020-06-22

Abstract: Mitochondrial complex I regenerates NAD+ and proton pumps for TCA cycle function andATP production, respectively. Mitochondrial complex I dysfunction has been implicatedin many brain pathologies including Leigh syndrome and Parkinson’s disease. We soughtto determine whether NAD+ regeneration or proton pumping, i.e., bioenergetics, isthe dominant function of mitochondrial complex I in protection from brain pathology.We generated a mouse that conditionally expresses the yeast NADH dehydrogenase (NDI1),a single enzyme that can replace the NAD+ regeneration capability of the 45-subunitmammalian mitochondrial complex I without proton pumping. NDI1 expression was sufficientto dramatically prolong lifespan without significantly improving motor function ina mouse model of Leigh syndrome driven by the loss of NDUFS4, a subunit of mitochondrialcomplex I. Therefore, mitochondrial complex I activity in the brain supports organismalsurvival through its NAD+ regeneration capacity, while optimal motor control requiresthe bioenergetic function of mitochondrial complex I.

DOI: 10.1016/j.cmet.2020.06.003

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30304-1

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