Title : Critical Role of Astrocyte NAD+ Glycohydrolase in Myelin Injury and Regeneration.

Pub. Date : 2021 Oct 13

PMID : 34493542






9 Functional Relationships(s)
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1 CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS. NAD CD38 antigen Mus musculus
2 CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS. NAD CD38 antigen Mus musculus
3 CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS. NAD CD38 antigen Mus musculus
4 CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS. NAD CD38 antigen Mus musculus
5 We demonstrate that CD38-catalytically inactive mice are substantially protected from high fat-induced NAD+ depletion, oligodendrocyte loss, oxidative damage, and astrogliosis. NAD CD38 antigen Mus musculus
6 A CD38 inhibitor, 78c, increased NAD+ and attenuated neuroinflammatory changes induced by saturated fat applied to astrocyte cultures. NAD CD38 antigen Mus musculus
7 Our findings suggest high fat diet impairs oligodendrocyte survival and differentiation through astrocyte-linked mechanisms mediated by the NAD+ase CD38 and highlight CD38 inhibitors as potential therapeutic candidates to improve myelin regeneration.SIGNIFICANCE STATEMENTMyelin disturbances and oligodendrocyte loss can leave axons vulnerable leading to permanent neurologic deficits. NAD CD38 antigen Mus musculus
8 We demonstrate that restoring nicotinamide adenine dinucleotide (NAD+) levels via genetic inactivation of CD38 can overcome these effects. NAD CD38 antigen Mus musculus
9 We demonstrate that restoring nicotinamide adenine dinucleotide (NAD+) levels via genetic inactivation of CD38 can overcome these effects. NAD CD38 antigen Mus musculus