Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12774044_1.fastq.gz | Fastqsanger.gz | |||
| SRR12774044_2.fastq.gz | Fastqsanger.gz | |||
| SRR12774045_1.fastq.gz | Fastqsanger.gz | |||
| SRR12774045_2.fastq.gz | Fastqsanger.gz | |||
| SRR12774046_1.fastq.gz | Fastqsanger.gz |
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Project description:Given the salient role of early-life adversity (ELA) and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
2023-03-21 | GSE227812 | GEO
Project description:Given the salient role of early-life adversity and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
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Project description:Late-life intervention with a soy-enriched diet attenuated age-dependent changes in renal structure and dysfunction in male Fischer 344 rats.
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Project description:Intergenerational stress increases lifetime susceptibility to depression and other psychiatric disorders. Whether intergenerational stress transmission is a consequence of in-utero neurodevelopmental disruptions or early-life mother-infant interaction is largely unknown, due to the complexity, superposition, and inseparability between the prenatal and postnatal mechanisms. Here we show that prenatal stress, through exposing pregnant mice to predator scent, induces depressive-like behavior and social deficits. Cross-fostering experiments indicate divergent and convergent mechanisms of both in utero and early-life parenting environments and support a two-hit model of stress transmission. According to this model, prenatal stress (first-hit) primes brain metabolome and transcriptome (metabotranscriptome), and increases vulnerability to the second-hit in early life, triggered by poor caregiving by the traumatized mothers. Metabolomics, transcriptomic and bioinformatics analyses reveal mechanisms that involve stress- and hypoxia- response metabolic pathways in the brains of the newborn mice, likely through the production of the epigenetic modifiers 2-Hydroxyglutaric acid and succinic acid. These responses produce long-lasting alterations in mitochondrial-energy metabolism, and epigenetic processes pertaining to DNA and chromatin modifications. We demonstrate that an early pharmacological intervention – correction of the mitochondria metabolism, and epigenetic modifications with acetyl-L-carnitine (ALCAR) supplementation - produces long-lasting protection against the behavioral deficits associated with intergenerational transmission of traumatic stress.
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