منابع مشابه
Boosting NAD to spare hearing.
Ex vivo experiments have strangely shown that inhibition or stimulation of NAD metabolism can be neuroprotective. In this issue of Cell Metabolism, Brown et al. (2014) demonstrate that cochlear NAD is diminished by deafening noise but protected by nicotinamide riboside or WldS mutation. Hearing protection by nicotinamide riboside depends on Sirt3.
متن کاملBoosting NAD+ for the prevention and treatment of liver cancer
Hepatocellular carcinoma (HCC) is the third leading cause of cancer death worldwide yet has limited therapeutic options. We recently demonstrated that inhibition of de novo nicotinamide adenine dinucleotide (NAD(+)) synthesis is responsible for DNA damage, thereby initiating hepatocarcinogenesis. We propose that boosting NAD(+) levels might be used as a prophylactic or therapeutic approach in HCC.
متن کاملCognitive spare capacity in older adults with hearing loss
Individual differences in working memory capacity (WMC) are associated with speech recognition in adverse conditions, reflecting the need to maintain and process speech fragments until lexical access can be achieved. When working memory resources are engaged in unlocking the lexicon, there is less Cognitive Spare Capacity (CSC) available for higher level processing of speech. CSC is essential f...
متن کاملPharmacological NAD-Boosting Strategies Improve Mitochondrial Homeostasis in Human Complex I-Mutant Fibroblasts.
Mitochondrial disorders are devastating genetic diseases for which efficacious therapies are still an unmet need. Recent studies report that increased availability of intracellular NAD obtained by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cell Metabolism
سال: 2014
ISSN: 1550-4131
DOI: 10.1016/j.cmet.2014.11.015