Abstract
Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While CD38 is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by CD38 in neurodegeneration and neuroinflammation remains elusive. Yet, CD38 expression increases as a consequence of aging which is otherwise the primary risk associated with neurodegenerative diseases, and several experimental data demonstrated that CD38 knockout mice are protected from neurodegenerative and neuroinflammatory insults. Moreover, nicotinamide adenine dinucleotide, whose levels are tightly controlled by CD38, is a recognized and potent neuroprotective agent, and NAD supplementation was found to be beneficial against neurodegenerative diseases. The aims of this review are to summarize the physiological role played by CD38 in the brain, present the arguments indicating the involvement of CD38 in neurodegeneration and neuroinflammation, and to discuss these observations in light of CD38 complex biology.
Highlights
Neurodegenerative diseases (NDDs) refer to conditions in which neurons in the central or peripheral nervous system degenerate
nicotinamide adenine dinucleotide (NAD) levels were found to decrease as a consequence of aging [6], including in the human brain and cerebrospinal fluid (CSF) [7,8], while NAD was found to be a potent neuroprotective and anti-inflammatory molecule [9]
The aims of this review are to summarize the physiological role played by CD38 in the brain, to discuss whether CD38 is involved in neurodegeneration and neuroinflammation, and to present how to interpret experimental data in view of CD38 complex biology
Summary
Neurodegenerative diseases (NDDs) refer to conditions in which neurons in the central or peripheral nervous system degenerate. While the process by which neurons undergo degeneration remains elusive, it appears to be multifactorial at the cellular level. It is tempting to study age-related dysfunctions that could favor or be instrumental in the neurodegenerative process. Reduced nicotinamide adenine dinucleotide (NAD) levels might be one of these age-related dysfunctions influencing neurodegeneration [5]. NAD levels were found to decrease as a consequence of aging [6], including in the human brain and cerebrospinal fluid (CSF) [7,8], while NAD was found to be a potent neuroprotective and anti-inflammatory molecule [9]. CD38 deletion was found to repress neurodegeneration and neuroinflammation in experimental models of NDDs. CD38 biology is complex and not restricted to its NAD-degrading ability [12]. The aims of this review are to summarize the physiological role played by CD38 in the brain, to discuss whether CD38 is involved in neurodegeneration and neuroinflammation, and to present how to interpret experimental data in view of CD38 complex biology
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