ArticleAnnals of neurology2015
Alzheimer's disease pathology is attenuated in a CD38-deficient mouse model.
Article in Annals of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Anticancer drugs repurposed for Alzheimer's disease: a systematic review.Alzheimer's research & therapy · 2021Pooled it
- Emerging chemical strategies for CD38 inhibition: restoring NADBioorganic & medicinal chemistry · 2026Review
- NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Abi3Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Unravelling Synaptic and Metabolic Mechanisms of Cognitive Resilience in Asymptomatic Alzheimer's Disease Across Two Alzheimer's Disease Cohorts.Cellular and molecular neurobiology · 2026Article
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- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Glomerular endothelial cells eliminate nicotinamide adenine dinucleotide to instruct CD103Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.Molecular neurobiology · 2025Review
- REV-ERBα regulates brain NADNature aging · 2025Article
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- The role of NADnpj metabolic health and disease · 2025Review
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Targeting CD38 immunometabolic checkpoint improves metabolic fitness and cognition in a mouse model of Alzheimer's disease.Nature communications · 2025Article
- Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents.Scientific reports · 2025Article
- The potential of olfaction loss to induce cognitive impairment and anxiety behavior in mice via the microbiota-gut-brain axis.Frontiers in microbiology · 2025Article
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- Article
- Article
- Nicotinamide Adenine Dinucleotide Does Not Improve Anesthetic Recovery in Rodents.Research square · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveAlzheimer's disease (AD)-associated dementia is due to tissue damage caused by amyloid β (Aβ) deposition within the brain and by accompanying neuroinflammation. The nicotinamide adenine dinucleotide (NAD) glycohydrolase CD38, which is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair processes in the brain and other tissues by degrading NAD and repressing the activity of other NAD-consuming enzymes and by producing NAD-derived metabolites that regulate calcium signaling and migration of inflammatory cells. Given the role of CD38 in neuroinflammation and repair, we examined the effect of CD38 deletion on AD pathology.
methodsWe crossed APPswePS1ΔE9 (APP.PS) mice with Cd38(-) (/) (-) mice to generate AD-prone CD38-deficient animals (APP.PS.Cd38(-) (/) (-) ) and examined AD-related phenotypes in both groups.
resultsAPP.PS.Cd38(-) (/) (-) mice exhibited significant reductions in Aβ plaque load and soluble Aβ levels compared to APP.PS mice, and this correlated with improved spatial learning. Although CD38 deficiency resulted in decreased microglia/macrophage (MM) accumulation, the transcription profile of the Cd38(-) (/) (-) and Cd38(+/) (+) MM was similar, suggesting that the decreased Aβ burden in APP.PS.Cd38(-) (/) (-) mice was not due to alterations in MM activation/function. Instead, APP.PS.Cd38(-) (/) (-) neuronal cultures secreted less Aβ and this reduction was mimicked when APP.PS neuronal cultures were treated with inhibitors that blocked CD38 enzyme activity or the signaling pathways controlled by CD38-derived metabolites. Furthermore, β- and γ-secretase activity was decreased in APP.PS.Cd38(-) (/) (-) mice, which correlated with decreased Aβ production.
interpretationCD38 regulates AD pathology in the APP.PS model of AD, suggesting that CD38 may be a novel target for AD treatment.
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