NAD+ in aging, metabolism, and neurodegeneration

By E. Verdin. Science, 2015

1,199 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/e360a313c46f8e83b376139c93549447ab1422ae

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Geriatrics and Gerontology

1. Ping Gao
2. Guido Kroemer
3. P. Jat
4. Huafeng Zhang
5. R. Kumari
6. Linchong Sun

In Oncology

1. L. Galluzzi
2. Guido Kroemer
3. C. López‐Otín
4. Ping Gao
5. P. Jat
6. Huafeng Zhang
7. R. Kumari
8. Linchong Sun

In Physiology

1. L. Galluzzi
2. Guido Kroemer
3. C. López‐Otín
4. Ping Gao
5. P. Jat
6. Evandro Fei Fang
7. Huafeng Zhang
8. R. Kumari

Citations in the corpus

• Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “In addition to SIRTs, there are several other NAD+-dependent enzymes involved in neuronal stress responses including poly (ADP -ribose) polymerase 1 (PARP1), cyclic ADP ribose hydrolase (CD38), and CD157 [89].”
• Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “NAD+ is mainly synthesized from the tryptophan, Preiss-Handler, or nicotinamide (NAM) salvage pathways, with the latter pathway contributing the majority of NAD+ (Verdin, 2015; Yang and Sauve, 2016).”
• NAD+ intermediates: The biology and therapeutic potential of NMN and NR (2017, neutral): “In addition, accumulating evidence suggests that NAD+ levels decline with age at a systemic level in diverse organisms, including rodents and humans, contributing to the development of many age-associated pathophysiologies (Canto et al., 2015; Imai and Guarente, 2014; Verdin, 2015).”
• Metabolic Control of Longevity. (2016, background): “The mechanisms accounting for NAD+ loss are presumably multifactorial, encompassing downregulation of the biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT), hyperactivation of the NAD+-consuming enzyme PARP1, disruption of circadian rhythms, and chronic inflammation (Verdin, 2015).”
• Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021, background): “Nicotinamide phosphoribosyl transferase (NAMPT) catalyzes the rate limiting step in the NAD salvage pathway from nicotinamide (NAM) (Garten et al., 2015; Verdin, 2015).”