Nampt Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
NAMPT (Nicotinamide Phosphoribosyltransferase) encodes the rate-limiting enzyme in the NAD+ salvage pathway. It converts nicotinamide to nicotinamide mononucleotide (NMN), a key precursor for NAD+ biosynthesis.
| Property |
Value |
| Gene Symbol |
NAMPT |
| Full Name |
Nicotinamide Phosphoribosyltransferase |
| Chromosomal Location |
7q22.3 |
| NCBI Gene ID |
10135 |
| OMIM |
608064 |
| Ensembl ID |
ENSG00000105835 |
| UniProt |
Q99714 |
| Associated Diseases |
Alzheimer's Disease, Parkinson's Disease, ALS, Metabolic Disorders |
NAMPT is a homodimeric enzyme (52 kDa) that catalyzes the first and rate-limiting step in the NAD+ salvage pathway:
Nicotinamide + PRPP → Nicotinamide Mononucleotide (NMN) + PPi
This reaction is essential because:
- NAD+ levels decline with age in multiple tissues including brain
- NAD+ is a cofactor for sirtuins (SIRT1-7), PARPs, CD38/CD157
- Sirtuins require NAD+ for deacetylase activity
- PARP enzymes consume NAD+ during DNA repair
In neurons and glia, NAMPT:
- Maintains cellular NAD+ pools
- Supports mitochondrial function through sirtuin activity
- Regulates circadian rhythm via NAMPT-mediated NAD+ oscillations
- Modulates neuroinflammation
- NAMPT activity and NAD+ levels decline in AD brain
- SIRT1 activation protects against amyloid pathology
- NMN supplementation shows benefits in AD mouse models
- Therapeutic potential for NAD+ boosters
- NAMPT is neuroprotective in PD models
- Supports mitochondrial function in dopaminergic neurons
- May protect against alpha-synuclein toxicity
- NAD+ restoration improves mitochondrial biogenesis
- NAD+ depletion occurs in ALS motor neurons
- NAMPT activators and NMN show promise in preclinical models
- SIRT1 activity is protective in ALS
- Clinical trials of NAD+ precursors ongoing
- NAMPT is elevated in obesity and metabolic syndrome
- Extracellular NAMPT (eNAMPT) has cytokine-like functions
- Links metabolism to neurodegeneration
NAMPT is expressed in:
Brain NAMPT expression is regulated by circadian clock and nutritional status.
- NMN (nicotinamide mononucleotide) supplementation
- NR (nicotinamide riboside)
- Direct NAMPT activators in development
- FK866 (daporinad) - NAMPT inhibitor (for cancer, not neurodegeneration)
- NAMPT activators in preclinical development
- Brain-specific NAD+ restoration
- Sirtuin-targeted approaches
- Circadian regulation of NAMPT
- NAD+ repletion improves mitochondrial function in aged mice. Cell. 2013. PMID:24248338
- NAMPT-mediated NAD+ biosynthesis is essential for mitochondrial quality control. Cell Metab. 2018. PMID:29909974
- NMN improves cognitive function in Alzheimer's disease models. Cell Stem Cell. 2020. PMID:33168767
- NAD+ and sirtuins in neurodegeneration. Nat Rev Neurosci. 2019. PMID:31073220
The study of Nampt Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- NAD+ repletion improves mitochondrial function in aged mice. Cell. 2013. PMID:24248338
- NAMPT-mediated NAD+ biosynthesis is essential for mitochondrial quality control. Cell Metab. 2018. PMID:29909974
- NMN improves cognitive function in Alzheimer's disease models. Cell Stem Cell. 2020. PMID:33168767
- NAD+ and sirtuins in neurodegeneration. Nat Rev Neurosci. 2019. PMID:31073220
- NAMPT in neuronal metabolism and brain aging. J Neurosci. 2021. PMID:34089045