ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Expression of Nampt in hippocampal and cortical excitatory neurons is critical for cognitive function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Neuronal C/EBPβ Shortens the Lifespan via Inactivating NAMPT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- Roles of NADCold Spring Harbor perspectives in medicine · 2024Review
- Axonal energy metabolism, and the effects in aging and neurodegenerative diseases.Molecular neurodegeneration · 2023Review
- Role of NADCellular and molecular neurobiology · 2023Review
- Interactions between Intestinal Homeostasis and NADNutrients · 2023Review
- Oral Administration of Nicotinamide Mononucleotide Increases Nicotinamide Adenine Dinucleotide Level in an Animal Brain.Nutrients · 2022Article
- Extracellular Nicotinamide Phosphoribosyltransferase Is a Component of the Senescence-Associated Secretory Phenotype.Frontiers in endocrinology · 2022Article
- Preoperative plasma visfatin may have a dual effect on the occurrence of postoperative delirium.Frontiers in medicine · 2022Article
- Cognitive deficits and impaired hippocampal long-term potentiation in KProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Nicotinamide phosphoribosyltransferase inhibitor ameliorates mouse aging-induced cognitive impairment.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Metabolomic and transcriptional profiling reveals bioenergetic stress and activation of cell death and inflammatory pathwaysJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Nicotinamide Mononucleotide Prevents Cisplatin-Induced Cognitive Impairments.Cancer research · 2021Article
- Mitochondrial and Autophagic Regulation of Adult Neurogenesis in the Healthy and Diseased Brain.International journal of molecular sciences · 2021Review
- Using animal models to evaluate the functional consequences of anesthesia during early neurodevelopment.Neurobiology of learning and memory · 2019Review
- NADCell metabolism · 2019Review
- Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice.Cell metabolism · 2019Article
- Role of endothelial NADAmerican journal of physiology. Heart and circulatory physiology · 2019Review
- Combined SIRT3 and SIRT5 deletion is associated with inner retinal dysfunction in a mouse model of type 1 diabetes.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Nicotinamide adenine dinucleotide (NAD(+)) is an enzyme cofactor or cosubstrate in many essential biological pathways. To date, the primary source of neuronal NAD(+) has been unclear. NAD(+) can be synthesized from several different precursors, among which nicotinamide is the substrate predominantly used in mammals. The rate-limiting step in the NAD(+) biosynthetic pathway from nicotinamide is performed by nicotinamide phosphoribosyltransferase (Nampt). Here, we tested the hypothesis that neurons use intracellular Nampt-mediated NAD(+) biosynthesis by generating and evaluating mice lacking Nampt in forebrain excitatory neurons (CaMKIIαNampt(-/-) mice). CaMKIIαNampt(-/-) mice showed hippocampal and cortical atrophy, astrogliosis, microgliosis, and abnormal CA1 dendritic morphology by 2-3 months of age. Importantly, these histological changes occurred with altered intrahippocampal connectivity and abnormal behavior; including hyperactivity, some defects in motor skills, memory impairment, and reduced anxiety, but in the absence of impaired sensory processes or long-term potentiation of the Schaffer collateral pathway. These results clearly demonstrate that forebrain excitatory neurons mainly use intracellular Nampt-mediated NAD(+) biosynthesis to mediate their survival and function. Studying this particular NAD(+) biosynthetic pathway in these neurons provides critical insight into their vulnerability to pathophysiological stimuli and the development of therapeutic and preventive interventions for their preservation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.