CD38 in Neurodegeneration and Neuroinflammation

Guerreiro, Serge; Privat, Anne-Laure; Bressac, Laurence; Toulorge, Damien

doi:10.3390/cells9020471

Cited by 97 publications

(81 citation statements)

References 75 publications

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“…Given its role in regulation of neuroinflammatory and brain repair processes, the effect of depletion of CD38, a NAD glycohydrolase expressed by neurons, astrocytes and microglial cells, by daratumumab has been evaluated in the AD context (Guerreiro et al, 2020).…”

Section: Daratumumab (Cd38)mentioning

confidence: 99%

“…As mentioned above, CD38 is a multifunctional protein with both a receptor and an enzyme-mediated function involved in several important reactions for the physiological neuronal development (Guerreiro et al, 2020).…”

Section: Daratumumab (Nct04070378)mentioning

confidence: 99%

“…CD38 expression increases during neuroinflammation and neurodegeneration, suggesting its potential modulating role in brain cells regulation. Experiments on CD38 knockout mice (Roboon et al, 2019), demonstrated a decreased release of pro-inflammatory cytokines and chemokines (Kou et al, 2009), while its overexpression was found after treatment with drugs-induced neuroinflammation (Guerreiro et al, 2020).…”

Section: Daratumumab (Nct04070378)mentioning

confidence: 99%

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Repositioning of Immunomodulators: A Ray of Hope for Alzheimer’s Disease?

et al. 2020

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Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder characterized by cognitive decline and by the presence of amyloid β plaques and neurofibrillary tangles in the brain. Despite recent advances in understanding its pathophysiological mechanisms, to date, there are no disease-modifying therapeutic options, to slow or halt the evolution of neurodegenerative processes in AD. Current pharmacological treatments only transiently mitigate the severity of symptoms, with modest or null overall improvement. Emerging evidence supports the concept that AD is affected by the impaired ability of the immune system to restrain the brain’s pathology. Deep understanding of the relationship between the nervous and the immune system may provide a novel arena to develop effective and safe drugs for AD treatment. Considering the crucial role of inflammatory/immune pathways in AD, here we discuss the current status of the immuno-oncological, immunomodulatory and anti-TNF-α drugs which are being used in preclinical studies or in ongoing clinical trials by means of the drug-repositioning approach.

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Section: Daratumumab (Cd38)mentioning

confidence: 99%

Section: Daratumumab (Nct04070378)mentioning

confidence: 99%

Section: Daratumumab (Nct04070378)mentioning

confidence: 99%

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Repositioning of Immunomodulators: A Ray of Hope for Alzheimer’s Disease?

et al. 2020

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“…Because no reports of middle-aged CD157 KO mice exist to our knowledge, it is not possible to compare our current results with other reports. However, aging effects in CD38 KO mice have been well studied [36,44], but these mice were produced on an ICR genetic background. Few reports are available regarding aging in the ICR strain [1,6,40].…”

Section: Discussionmentioning

confidence: 99%

Distinct physical condition and social behavior phenotypes of CD157 and CD38 knockout mice during aging

Gerasimenko

Lopatina²,

Shabalova

et al. 2020

Preprint

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The ability of CD38 and CD157 to consume nicotinamide adenine dinucleotide (NAD) has received much attention because aging-induced elevation of CD38 expression plays a role in the senescence-related decline in NAD levels. Therefore, it is of interest to examine and compare the effects of age-associated changes on the general health and brain function impairment of Cd157 and Cd38 knockout (CD157 KO and CD38 KO) mice. Body weight and behaviors were measured in 8-week-old (young adult) or 12-month-old (middle-aged) male mice of both KO strains. The locomotor activity, anxiety-like behavior, and social behavior of mice were measured in open field, and three-chamber tests. Middle-aged CD157 KO male mice gained more body weight than young adult mice, while little or no body weight gain was observed in middle-aged CD38 KO mice. Middle-aged CD157 KO mice displayed increased anxiety-like behavior and decreased sociability and interaction compared with young adult KO mice. Middle-aged CD38 KO mice showed less anxiety and hyperactivity than CD157 KO mice, similar to young adult CD38 KO mice. The results reveal marked age-dependent changes in male CD157 KO mice but not in male CD38 KO mice. We discuss the distinct differences in aging effects from the perspective of inhibition of NAD metabolism in CD157 and CD38 KO mice, which may contribute to differential behavioral changes during aging.

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“…In addition to its role in obesity, CD38 is also expressed in neurons, microglial cells, and astrocytes [reviewed in Guerreiro et al (2020) ]. CD38 is highly expressed in the mouse brain during development (postnatal days 14 and 28).…”

Section: Genes Associated With Obesity and Neurodegenerative And Neurmentioning

confidence: 99%

Environment and Gene Association With Obesity and Their Impact on Neurodegenerative and Neurodevelopmental Diseases

2020

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Obesity is a multifactorial disease in which environmental conditions and several genes play an important role in the development of this disease. Obesity is associated with neurodegenerative diseases (Alzheimer, Parkinson, and Huntington diseases) and with neurodevelopmental diseases (autism disorder, schizophrenia, and fragile X syndrome). Some of the environmental conditions that lead to obesity are physical activity, alcohol consumption, socioeconomic status, parent feeding behavior, and diet. Interestingly, some of these environmental conditions are shared with neurodegenerative and neurodevelopmental diseases. Obesity impairs neurodevelopment abilities as memory and fine-motor skills. Moreover, maternal obesity affects the cognitive function and mental health of the offspring. The common biological mechanisms involved in obesity and neurodegenerative/neurodevelopmental diseases are insulin resistance, pro-inflammatory cytokines, and oxidative damage, among others, leading to impaired brain development or cell death. Obesogenic environmental conditions are not the only factors that influence neurodegenerative and neurodevelopmental diseases. In fact, several genes implicated in the leptin–melanocortin pathway ( LEP , LEPR , POMC , BDNF , MC4R , PCSK1 , SIM1 , BDNF , TrkB , etc.) are associated with obesity and neurodegenerative and neurodevelopmental diseases. Moreover, in the last decades, the discovery of new genes associated with obesity ( FTO, NRXN3, NPC1, NEGR1, MTCH2, GNPDA2 , among others) and with neurodegenerative or neurodevelopmental diseases ( APOE, CD38, SIRT1, TNF α, PAI-1, TREM2, SYT4, FMR1, TET3 , among others) had opened new pathways to comprehend the common mechanisms involved in these diseases. In conclusion, the obesogenic environmental conditions, the genes, and the interaction gene–environment would lead to a better understanding of the etiology of these diseases.

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CD38 in Neurodegeneration and Neuroinflammation

Cited by 97 publications

References 75 publications

Repositioning of Immunomodulators: A Ray of Hope for Alzheimer’s Disease?

Repositioning of Immunomodulators: A Ray of Hope for Alzheimer’s Disease?

Distinct physical condition and social behavior phenotypes of CD157 and CD38 knockout mice during aging

Environment and Gene Association With Obesity and Their Impact on Neurodegenerative and Neurodevelopmental Diseases

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