Decreased NAD+ in dopaminergic neurons

Sison, Samantha L; Ebert, Allison D.

doi:10.18632/aging.101433

Cited by 3 publications

(3 citation statements)

References 7 publications

(8 reference statements)

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“…As evidenced, neurons expressing the LRRK2 G2019S mutation exhibit mitochondrial dysfunction and a 30% reduction of NAD + levels. Interestingly, this mutation seems to specifically affect dopaminergic neurons, since no mitochondrial dysfunction or NAD + reduction was observed in glutamatergic or sensory neurons expressing the mutation (Schwab et al, 2017;Sison and Ebert, 2018). Mitochondrial impairments in dopaminergic neurons expressing mutant LRRK2 include decreased mitochondrial mass, aberrant subcellular distribution of mitochondria, altered mitochondrial respiration and ATP levels, and impaired mitochondrial motility (Schwab et al, 2017;Sison and Ebert, 2018).…”

Section: Nad + Depletion and Dysregulation Of Neuronal Calciummentioning

confidence: 99%

“…Interestingly, this mutation seems to specifically affect dopaminergic neurons, since no mitochondrial dysfunction or NAD + reduction was observed in glutamatergic or sensory neurons expressing the mutation (Schwab et al, 2017;Sison and Ebert, 2018). Mitochondrial impairments in dopaminergic neurons expressing mutant LRRK2 include decreased mitochondrial mass, aberrant subcellular distribution of mitochondria, altered mitochondrial respiration and ATP levels, and impaired mitochondrial motility (Schwab et al, 2017;Sison and Ebert, 2018). Dopaminergic neurons derived from iPSCs expressing mutant GBA exhibit a reduced cytosolic NAD + /NADH ratio, although no significant change of total cellular NAD + was seen (Schö ndorf et al, 2018).…”

Section: Nad + Depletion and Dysregulation Of Neuronal Calciummentioning

confidence: 99%

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NAD+ in Brain Aging and Neurodegenerative Disorders

et al. 2019

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NAD + is a pivotal metabolite involved in cellular bioenergetics, genomic stability, mitochondrial homeostasis, adaptive stress responses, and cell survival. Multiple NAD + -dependent enzymes are involved in synaptic plasticity and neuronal stress resistance. Here, we review emerging findings that reveal key roles for NAD + and related metabolites in the adaptation of neurons to a wide range of physiological stressors and in counteracting processes in neurodegenerative diseases, such as those occurring in Alzheimer's, Parkinson's, and Huntington diseases, and amyotrophic lateral sclerosis. Advances in understanding the molecular and cellular mechanisms of NAD + -based neuronal resilience will lead to novel approaches for facilitating healthy brain aging and for the treatment of a range of neurological disorders.

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Section: Nad + Depletion and Dysregulation Of Neuronal Calciummentioning

confidence: 99%

Section: Nad + Depletion and Dysregulation Of Neuronal Calciummentioning

confidence: 99%

NAD+ in Brain Aging and Neurodegenerative Disorders

et al. 2019

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“…In macrophages, SIRT regulates mitochondrial function through the deacetylation of complex I and plays a key role in enhancing antioxidant activity and resisting the increase in mitochondrial ROS [ 120 ]. Since it depends on NAD to function, the protective effect of SIRT is significantly weaker in dopaminergic neurons [ 121 ].…”

Section: Microbial Metabolites and Mitochondrial Dysfunction In Pd: Is There A Link?mentioning

confidence: 99%

Gut Microbial Metabolites in Parkinson’s Disease: Implications of Mitochondrial Dysfunction in the Pathogenesis and Treatment

et al. 2021

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The search for therapeutic targets for Parkinson’s disease (PD) is hindered by the incomplete understanding of the pathophysiology of the disease. Mitochondrial dysfunction is an area with high potential. The neurobiological signaling connections between the gut microbiome and the central nervous system are incompletely understood. Multiple lines of evidence suggest that the gut microbiota participates in the pathogenesis of PD. Gut microbial dysbiosis may contribute to the loss of dopaminergic neurons through mitochondrial dysfunction. The intervention of gut microbial metabolites via the microbiota-gut-brain axis may serve as a promising therapeutic strategy for PD. In this narrative review, we summarize the potential roles of gut microbial dysbiosis in PD, with emphasis on microbial metabolites and mitochondrial function. We then review the possible ways in which microbial metabolites affect the central nervous system, as well as the impact of microbial metabolites on mitochondrial dysfunction. We finally discuss the possibility of gut microbiota as a therapeutic target for PD.

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Decreased NAD+ in dopaminergic neurons

Cited by 3 publications

References 7 publications

NAD+ in Brain Aging and Neurodegenerative Disorders

NAD+ in Brain Aging and Neurodegenerative Disorders

Gut Microbial Metabolites in Parkinson’s Disease: Implications of Mitochondrial Dysfunction in the Pathogenesis and Treatment

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