2016 Oct 11;24(4):526-528. doi: 10.1016/j.cmet.2016.09.019.

Author information

1
Novartis Professor, Koch Institute Affiliate and Director of the Paul F. Glenn Center for the Science of Aging Research, MIT, Cambridge, MA 02139, USA. Electronic address: leng@mit.edu.

Abstract

In this issue, Fang et al. (2016) show that both the DNA repair defect and mitochondrial dysfunction in ATM-/- cells or mice are mitigated by the anti-aging compound nicotinamide riboside or a SIRT1 activator. This broad suppression by activating the NAD+/SIRT1 axis may generally apply to diseases and aging maladies.

PMID:
 
27732834
 
DOI:
 
10.1016/j.cmet.2016.09.019
[Indexed for MEDLINE] 
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