Temporal Genomics Mechanisms Underlying Disease and Aging [DNA Methylation]
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ABSTRACT:
PROVIDER: PRJNA947125 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Temporal Genomics Mechanisms Underlying Disease and Aging
| PRJNA947120 | ENA
Project description:Temporal Genomics Mechanisms Underlying Disease and Aging [RNA-Seq]
| PRJNA947124 | ENA
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.
2023-03-21 | GSE227809 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-03-21 | GSE227815 | GEO
Project description:Gene expression profile suggests different mechanisms underlying sporadic and familial mesial temporal lobe epilepsy
| PRJNA834678 | ENA
Project description:Aging alters mechanisms underlying voluntary movements in spinal motor neurons of mice, primates and humans.
| PRJNA941252 | ENA
Project description:Aging induces functional declines in the mammalian brain, increasing its vulnerability to cognitive impairments and neurodegenerative disorders. Among various interventions to slow aging and delay age-related diseases, caloric restriction (CR) consistently extends lifespan across species. However, the specific molecular and cellular mechanisms through which CR benefits the aging brain remain unclear. In this study, we performed spatiotemporal profiling of mouse brains to uncover detailed mechanisms underlying the anti-aging effects of CR. We analyzed the transcriptional states of over half million single cells from mouse brain samples across various ages and in response to CR treatment. Monitoring the dynamics of over 300 transcriptionally distinct cellular states, we captured the temporal dynamics of cellular states particularly vulnerable to aging and those rescued by CR (e.g., CR delays the expansion of inflammatory glia and preserves neurogenesis cells). Further spatial transcriptome analysis revealed gene expression and cellular dynamics across brain regions in aged mice upon CR treatment, uncovering region-specific anti-aging effects. In summary, our spatiotemporal mouse brain profiling delineated highly cell-type-specific molecular pathways in response to aging and CR, shedding light on the nuanced regulatory roles of CR across different cell types and brain regions.
2025-07-08 | GSE273038 | GEO
Project description:Single cell RNA sequencing reveals mechanisms underlying a senescence-like phenotype of Alveolar Macrophages during Aging
| PRJNA848750 | ENA
Project description:Spinal motor neurons have been implicated in the loss of motor function that occurs with advancing age. However, the cellular and molecular mechanisms that impair the function of these neurons during aging remain unknown. Here, we show that motor neurons do not die in old female and male mice, rhesus monkeys, and humans. Instead, these neurons selectively shed excitatory synaptic inputs throughout the soma and dendritic arbor during aging. By examining the translatome , we also show that aging alters the molecular composition of motor neurons in both male and female mice. Aging motor neurons present with changes in genes and molecular pathways with roles in glia-mediated synaptic pruning, and inflammation. They also exhibit changes in pathways with roles in axonal regeneration caused by axotomy and Amyotrophic Lateral Sclerosis (ALS). Thus, we have identified cellular and molecular mechanisms altered in aged motor neurons that could serve as therapeutic targets to preserve motor function during aging.
2023-03-09 | GSE226699 | GEO