Tier 3 — preclinical

Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle

Frederick DW, Loro E, Liu L, Davila A Jr, Chellappa K, Silverman IM, Quinn WJ 3rd, Gosai SJ, Tichy ED, Davis JG, Mourkioti F, Gregory BD, Dellinger RW, Redpath P, Migaud ME, Nakamaru-Ogiso E, Rabinowitz JD, Khurana TS, Baur JA
Cell metabolism 2016 24; 2; 269-282

Bibliography

PubMed
PMID 27508874
PubMed Central
PMC4985182
DOI
10.1016/j.cmet.2016.07.005
Funding
Indexed grant support includes NIAMS NIH HHS, NIDDK NIH HHS, NIA NIH HHS. The complete funding declaration is not specified in the accessible abstract.
Competing interests
A complete competing-interest declaration is not specified in the accessible publication information.

Study snapshot

DesignPreclinical animal study with supporting assays as applicable
ModelGenetically modified and aging mice
SampleMuscle-specific Nampt-depletion and aging mouse experiments
InterventionNR rescue and genetic maintenance of NAD+ metabolism
DurationDisease-rescue and aging protocols
EndpointsModel-specific physiological outcomes; Biochemical or functional measures reported in the study

What the study showed, in plain terms

Severe NAD+ depletion damaged mouse skeletal muscle, while NR rescued several deficits in the depletion model.

Key findings

Severe NAD+ depletion damaged mouse skeletal muscle, while NR rescued several deficits in the depletion model.

What this study can and cannot tell us

An induced biochemical deficiency is not equivalent to ordinary human aging or proof of benefit in people with adequate NAD+ status.

Related papers in the corpus

Tier 3
NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation
Ryu D et al. · Science translational medicine · 2016

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology