Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesis.

Komal Pekhale, Vinod Tiwari, Mansoor Hussain, Christy C Bridges, Deborah L Croteau, Moshe Levi, Avi Z Rosenberg, Briana Santo, Xiaoping Yang, Tomasz Kulikowicz, Xiaoxin X Wang, Jong-Hyuk Lee, Vilhelm A Bohr

DNA repair section, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.DNA repair section, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA. · pubmed

Paper

Abstract

Cockayne Syndrome (CS) is a premature aging disorder caused by mutations in the CSA and CSB genes involved in DNA metabolism and other cellular processes. CS patients display many features including premature aging, neurodegeneration, and kidney abnormalities. Nicotinamide dinucleotide (NAD

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that Cockayne syndrome mice exhibit defects in de novo NAD biosynthesis, which reflects human kidney disease. This research is relevant as it explores the underlying mechanisms of a premature aging disorder, potentially linking NAD metabolism to aging processes.

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