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The reverse transcriptase inhibitor 3TC modulates hippocampal transcriptome signatures of inflammation in tauopathy model mice

ABSTRACT: The reverse transcriptase inhibitor 3TC modulates hippocampal transcriptome signatures of inflammation in tauopathy model mice

PROVIDER: PRJNA1019331 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26126432_1.fastq.gz	Fastqsanger.gz
	SRR26126432_2.fastq.gz	Fastqsanger.gz
	SRR26126433_1.fastq.gz	Fastqsanger.gz
	SRR26126433_2.fastq.gz	Fastqsanger.gz
	SRR26126434_1.fastq.gz	Fastqsanger.gz

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The reverse transcriptase inhibitor 3TC modulates hippocampal transcriptome signatures of inflammation in tauopathy model mice

Project description:Reducing neuroinflammation, a main hallmark of brain aging and neurodegenerative diseases, is a promising strategy for improving cognitive function in these settings. The nucleoside reverse transcriptase inhibitor 3TC (Lamivudine) has been reported to improve cognitive function in old wild-type mice and in multiple mouse models of neurodegenerative disease, but the underlying mechanisms have not been comprehensively investigated. In the current study, we used transcriptomics to broadly characterize the effects of long-term supplementation with a human-equivalent therapeutic dose of 3TC on the hippocampal transcriptome in male and female rTg4510 mice (a commonly studied model of tauopathy-associated neurodegeneration). We found that tauopathy increased hippocampal transcriptomic signatures of neuroinflammation/immune activation, but 3TC treatment reversed many of these transcriptome changes. We also found that 3TC mitigated tauopathy-associated activation of several key transcription factors that contribute to neuroinflammation and immune activation, and several of these changes were correlated with improved recognition memory performance.Our findings suggest that 3TC exerts beneficial effects on the hippocampus in the context of tauopathy by modulating pathways associated with inflammation and immune response.

2024-05-13 | GSE243650 | GEO

The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction

Project description:Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer's disease. Major hallmarks of brain aging include neuroinflammation/immune activation and reduced neuronal health/function. These processes contribute to cognitive dysfunction (a key risk factor for Alzheimer's disease), but their upstream causes are incompletely understood. Age-related increases in transposable element (TE) transcripts might contribute to reduced cognitive function with brain aging, as the reverse transcriptase inhibitor 3TC reduces inflammation in peripheral tissues and TE transcripts have been linked with tau pathology in Alzheimer's disease. However, the effects of 3TC on cognitive function with aging have not been investigated. Here, in support of a role for TE transcripts in brain aging/cognitive decline, we show that 3TC: (a) improves cognitive function and reduces neuroinflammation in old wild-type mice; (b) preserves neuronal health with aging in mice and Caenorhabditis elegans; and (c) enhances cognitive function in a mouse model of tauopathy. We also provide insight on potential underlying mechanisms, as well as evidence of translational relevance for these observations by showing that TE transcripts accumulate with brain aging in humans, and that these age-related increases intersect with those observed in Alzheimer's disease. Collectively, our results suggest that TE transcript accumulation during aging may contribute to cognitive decline and neurodegeneration, and that targeting these events with reverse transcriptase inhibitors like 3TC could be a viable therapeutic strategy.

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Project description:Aging is the primary risk factor for the development of many chronic diseases, including dementia, cardiovascular disease, and diabetes. There is significant interest in identifying novel “geroprotective” agents, including by repurposing existing drugs, but such treatments may affect organ systems differently. One current example is the nucleoside reverse transcriptase inhibitor 3TC, which has been increasingly studied as a potential gerotherapeutic. Recent data suggest 3TC may reduce inflammation and improve cognitive function in older mice; however, the effects of 3TC on other tissues in aged animals are less well characterized. Here, we use transcriptomics (RNA-seq) and targeted metabolomics to investigate the influence of 3TC supplementation on skeletal muscle in older mice. We show that 3TC: (a) does not overtly affect muscle mass or functional/health markers; (b) largely reverses age-related changes in gene expression and metabolite signatures; and (c) is potentially beneficial for mitochondrial function in old animals via increases in antioxidant enzymes and decreases in mitochondrial reactive oxygen species. Collectively, our results suggest that, in addition to its protective effects in other tissues, 3TC supplementation does not have adverse effects in aged muscle and may even protect muscle/mitochondrial health in this context.

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The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction

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