NAD + Depletion Is Necessary and Sufficient forPoly(ADP-Ribose) Polymerase-1-Mediated Neuronal Death
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Poly(ADP-ribose)-1 (PARP-1) is a key mediator of cell death in excitotoxicity, ischemia, and oxidative stress. PARP-1 activation leads to cytosolic NAD + depletion and mitochondrial release of apoptosis-inducing factor (AIF), but the causal relationships between these two events have been difficult to resolve. Here, we examined this issue by using extracellular NAD + to restore neuronal NAD + levels after PARP-1 activation. Exogenous NAD + was found to enter neurons through P2X 7 -gated channels. Restoration of cytosolic NAD + by this means prevented the glycolytic inhibition, mitochondrial failure, AIF translocation, and neuron death that otherwise results from extensive PARP-1 activation. Bypassing the glycolytic inhibition with the metabolic substrates pyruvate, acetoacetate, or hydroxybutyrate also prevented mitochondrial failure and neuron death. Conversely, depletion of cytosolic NAD + with NAD + glycohydrolase produced a block in glycolysis inhibition, mitochondrial depolarization, AIF translocation, and neuron death, independent of PARP-1 activation. These results establish NAD + depletion as a causal event in PARP-1-mediated cell death and place NAD + depletion and glycolytic failure upstream of mitochondrial AIF release.
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PARP1 inhibitors have limited clinical use because of toxicity.
“They sensitize tumours to DNA damage, but they have limited use due to toxicity223–225.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [223]
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- Authors
- Alano, C. C., Garnier, P., Ying, W., Higashi, Y., Kauppinen, T. M., & Swanson, R. A.
- Affiliations
- San Francisco VA Medical Center (US)
- Corresponding author
- Alano, Conrad C.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-02-24
- Volume
- 30
- Issue
- 8
- Pages
- 2967-2978
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2864043
- OpenAlex
- W2074161856
- Cited by
- 439
- References
- 62
- Citations by year
- 2026: 16 · 2025: 21 · 2024: 18 · 2023: 28 · 2022: 20 · 2021: 30 · 2020: 29 · 2019: 29 · 2018: 26 · 2017: 39 · 2016: 28 · 2015: 37 · 2014: 25 · 2013: 33 · 2012: 30
- FWCI
- 11.99
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- American Heart Association
- National Institutes of Health (NS14543)
- National Institute of Neurological Disorders and Stroke (P50NS014543, NS-14543, P01NS014543)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- NAD+ depletion, PARP1, neuronal cell death, apoptosis-inducing factor, glycolysis inhibition, mitochondrial depolarization, NAD glycohydrolase, excitotoxicity, ischemia, oxidative stress, mitochondrial release
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, Animals, Cells, Cultured, Energy Metabolism, Glycolysis, Mitochondria, NAD, Nerve Degeneration, Neurons, Poly(ADP-ribose) Polymerases, Cell Death, Receptors, Purinergic P2, Mice, Knockout, Cell Respiration, Protein Transport, Mitochondrial Diseases, Apoptosis Inducing Factor, Mice, Receptors, Purinergic P2X7
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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