Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1115098 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29142407_1.fastq.gz | Fastqsanger.gz | |||
| SRR29142407_2.fastq.gz | Fastqsanger.gz | |||
| SRR29142408_1.fastq.gz | Fastqsanger.gz | |||
| SRR29142408_2.fastq.gz | Fastqsanger.gz | |||
| SRR29142409_1.fastq.gz | Fastqsanger.gz |
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Project description:Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer's disease (AD), but their role in disease-defining pathology is unclear. We developed a DNA repair-deficient 3xTgAD/Polb+/- mouse that exacerbates major features of human AD including pTau pathologies, synaptic dysfunction, neuronal death and cognitive impairment. Here we report that 3xTgAD/Polb+/- mice have reduced cerebral NAD+/NADH ratio indicating impaired cerebral energy metabolism, which is normalized by nicotinamide riboside (NR) treatment. NR lessened pTau pathology in both 3xTgAD and 3xTgAD/Polb+/- mice, but had no impact on Abeta accumulation. NR-treated 3xTgAD/Polb+/- mice exhibited reduced DNA damage, neuroinflammation, apoptosis of hippocampal neurons, and increased activity of SIRT3 in the brain. NR improves cognitive function in multiple behavioral tests, and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polb+/- mice. In general, the deficits and the benefits of NR were greater in 3xTgAD/Polb+/- mice than in 3xTgAD mice. Our findings suggest a pivotal role for cellular NAD+ depletion upstream of neuroinflammation, pTau, DNA damage, synaptic dysfunction and neuronal degeneration in AD. Interventions that bolster neuronal NAD+ levels therefore have potential in AD.
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Project description:The dysregulation of the microbiota-gut-brain axis (MGBA) in people living with HIV (PLWH) consequent to gastrointestinal dysfunction (dysbiosis) can lead to neuroinflammation and persistent cognitive impairment, which underscores the need for new treatments. Here, we show that delta-9-tetrahydrocannabinol (THC) reduced neuroinflammation and microbiome alterations and enhanced plasma endocannabinoid, endocannabinoid-like and indole-3-propionate levels in chronically SIV-infected rhesus macaques. Long-term low-dose THC potently blocked expression of genes associated with type I interferon responses and excitotoxicity (SLC7A11) and enhanced protein expression of WFS1 (endoplasmic reticulum stress) and CRYM (oxidative stress) in basal ganglia. Additionally, THC successfully countered miR-142-3p mediated suppression of WFS1 via a CB1R mediated mechanism in HCN2 neuronal cells. Most importantly, THC increased the relative abundance of Firmicutes and Clostridia including IPA producersing C. botulinum, C. paraputrificum, C. cadaveris and butyrate producersing C. butyricum, Faecalibacterium prauzsnitzii and Butyricicoccus pullicaecorum in the colon. This study highlights low-dose THC as a potential disease-modifying agent that can positively modulate the MGBA by concurrently reducing neuroinflammation and promoting the growth of gut microbial species that produce neuroprotective metabolites like indole-3-propionate in PLWH HIV and other neurodegenerative diseases, thus meriting clinical trials.
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Project description:This study investigates the roles of neurons, microglia, astrocytes, and oligodendrocytes in the pathogenesis of postoperative cognitive impairment, focusing on a dysregulated glia-neuron cycle. We utilized 18-month male C57BL/6 mice to model this condition, conducting single-cell RNA sequencing in the hippocampus to explore the neuroglial interactions and their implications in neuroinflammation, synaptic dysfunction, and myelin loss. This dataset includes transcriptomic profiles aimed at decoding the cellular communication in aged hippocampal cells and assessing the impact of therapeutic interventions on postoperative cognitive decline.
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