[Full Picture] NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer’s disease via cGAS–STING

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NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer’s disease via cGAS–STING - PMC

Source: ncbi.nlm.nih.gov

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Summary Analysis Research

Article summary:

1. Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disorder, and impaired neuronal bioenergetics and neuroinflammation are thought to play key roles in its progression.

2. Nicotinamide adenine dinucleotide (NAD+) levels are reduced in the brains of AD mice, and treatment with the NAD+ precursor nicotinamide riboside (NR) for 5 months increased brain NAD+ levels, reduced expression of proinflammatory cytokines, and decreased activation of microglia and astrocytes.

3. NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.

Article analysis:

This article is generally trustworthy as it provides evidence from multiple sources to support its claims. The authors cite relevant research studies to back up their assertions about the role of NAD+ in neurodegenerative diseases such as Alzheimer’s disease (AD). They also provide evidence from experiments conducted on transgenic mice with beta-amyloid pathology that demonstrate the beneficial effects of nicotinamide riboside (NR) supplementation on reducing inflammation, DNA damage, apoptosis, and cellular senescence in AD mouse brains. Furthermore, they discuss potential therapeutic targets for AD based on their findings.

However, there are some potential biases that should be noted. For example, the authors do not explore any possible risks associated with NR supplementation or present any counterarguments to their claims. Additionally, they do not provide any evidence for their assertion that cGAS–STING pathways are potential therapeutic targets for AD. Finally, while they discuss the role of NAD+ depletion-mediated activation of cGAS–STING in neuroinflammation and cellular senescence in AD, they do not explore other possible mechanisms by which NR supplementation may reduce inflammation or cell senescence in AD mouse brains.

Topics for further research:

Risks associated with nicotinamide riboside supplementation Counterarguments to NAD+ depletion-mediated activation of cGAS–STING in neuroinflammation Alternative mechanisms of NR supplementation in reducing inflammation in AD mouse brains Therapeutic targets for Alzheimer’s disease DNA damage in transgenic mice with beta-amyloid pathology Cellular senescence in Alzheimer’s disease