Nala GSI GSAv3 PGx Study
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001007710 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:A pilot study examining genetic determinants associated with elite long term non progression and rapid progression using exome sequencing of individuals at the extremes of the distribution of HIV control and progression. Data can only be used for HIV related research.
| EGAS00001000057 | EGA
Project description:The ability to form memories is a prerequisite for an organismâs behavioural adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell-types, and three time-points before and after contextual learning. Here we show that histone modifications predominantly change during memory acquisition and correlate surprisingly little with changes in gene expression. While long-lasting changes are almost exclusive to neurons, learning-related histone modification and DNA methylation changes occur also in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provides evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring. We examined chromatin modification changes in two distinct mouse brain regions (CA1 and ACC), two cell-types (neurons, non-neurons), and three time-points before and after contextual learning (naive, 1h, 4w).
2015-11-24 | E-GEOD-74966 | biostudies-arrayexpress
Project description:The ability to form memories is a prerequisite for an organismâs behavioural adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell-types, and three time-points before and after contextual learning. Here we show that histone modifications predominantly change during memory acquisition and correlate surprisingly little with changes in gene expression. While long-lasting changes are almost exclusive to neurons, learning-related histone modification and DNA methylation changes occur also in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provides evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring. We examined chromatin modification changes in two distinct mouse brain regions (CA1 and ACC), two cell-types (neurons, non-neurons), and three time-points before and after contextual learning (naive, 1h, 4w).
2015-11-24 | E-GEOD-74965 | biostudies-arrayexpress
Project description:Social communication guides decision making that is essential for survival. Social transmission of food preference (STFP) is an ecologically relevant memory paradigm in which an animal learns a desirable food odor from other animals in a social context. How food-preference memory is acquired, consolidated, and stored is unclear. Here, we identify a circuit involving the posteromedial nucleus of the cortical amygdala (COApm) as a computational center that integrates social and sensory olfactory inputs for long-term STFP memory consolidation. Blocking synaptic signaling by the COApm circuit selectively abolished STFP memory consolidation without impairing memory acquisition, storage, or recall. STFP memory consolidation by the COApm depends on synaptic inputs from the accessory olfactory bulb and on synaptic outputs to the anterior olfactory nucleus and requires protein synthesis, suggesting a gene expression mechanism. Deep single-cell and spatial transcriptomics revealed robust but distinct gene expression signatures induced by STFP memory formation in the COApm consistent with synapse restructuring. Our data thus define a neural circuit for consolidation of a socially communicated long-term memory, thereby mechanistically distinguishing protein synthesis-dependent memory consolidation from memory acquisition, storage, or retrieval.
2024-03-09 | GSE256522 | GEO
Project description:The circadian system influences many different biological processes, including memory performance. While the suprachiasmatic nucleus (SCN) functions as the brain’s central pacemaker, downstream “satellite clocks” may also regulate local functions based on the time of day. Within the dorsal hippocampus (DH), for example, local molecular oscillations may contribute to time-of-day effects on memory. Here, we used the hippocampus-dependent Object Location Memory task to determine how memory is regulated across the day/night cycle in mice. First, we systematically determined which phase of memory (acquisition, consolidation, or retrieval) is modulated across the 24h day. We found that mice show better long-term memory performance during the day than at night, an effect that was specifically attributed to diurnal changes in memory consolidation, as neither memory acquisition nor memory retrieval fluctuated across the day/night cycle. Using RNA-sequencing we identified the circadian clock gene Period1 (Per1) as a key mechanism capable of supporting this diurnal fluctuation in memory consolidation, as Per1 oscillates in tandem with memory performance. We then show that local knockdown of Per1 within the DH has no effect on either the circadian rhythm or sleep behavior, although previous work has shown this manipulation impairs memory. Thus, Per1 may independently function within the DH to regulate memory in addition to its known role in regulating the circadian system within the SCN. Per1 may therefore exert local diurnal control over memory consolidation within the DH.
2024-01-12 | GSE222744 | GEO
Project description:The ability to form memories is a prerequisite for an organism’s behavioural adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell-types, and three time-points before and after contextual learning. Here we show that histone modifications predominantly change during memory acquisition and correlate surprisingly little with changes in gene expression. While long-lasting changes are almost exclusive to neurons, learning-related histone modification and DNA methylation changes occur also in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provides evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring.
2015-11-24 | GSE74966 | GEO
Project description:The ability to form memories is a prerequisite for an organism’s behavioural adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell-types, and three time-points before and after contextual learning. Here we show that histone modifications predominantly change during memory acquisition and correlate surprisingly little with changes in gene expression. While long-lasting changes are almost exclusive to neurons, learning-related histone modification and DNA methylation changes occur also in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provides evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring.
2015-11-24 | GSE74964 | GEO
Project description:The ability to form memories is a prerequisite for an organism’s behavioural adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell-types, and three time-points before and after contextual learning. Here we show that histone modifications predominantly change during memory acquisition and correlate surprisingly little with changes in gene expression. While long-lasting changes are almost exclusive to neurons, learning-related histone modification and DNA methylation changes occur also in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provides evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring.
2015-11-24 | GSE74965 | GEO
Project description:Histone acetylation is a key component in the consolidation of long-term fear memories, which are models for highly resilient and durable memory. Histone acetylation is fueled by acetyl-CoA and recently, nuclear-localized metabolic enzymes that produce this metabolite have emerged as direct and local regulators of histone acetylation. In particular, Acetyl-coA synthetase 2 (ACSS2) mediates histone acetylation in the mouse hippocampus. However, whether ACSS2 regulates long-term fear memory remains to be determined. Here, we show that Acss2 knockout is well-tolerated in mice, yet the Acss2 null mouse exhibits reduced acquisition of long-term fear memory. Loss of Acss2 leads to reductions in both histone acetylation and expression of critical learning and memory-related genes in the dorsal hippocampus, specifically following fear conditioning. Further, systemic administration of blood-brain-barrier (BBB)-permeable Acss2 inhibitors during the consolidation window reduces fear memory formation in mice and rats, and reduces anxiety in a predator-scent-stress (PSS) paradigm. Our findings suggest that nuclear acetyl-CoA metabolism via ACSS2 plays a critical, previously unappreciated role in the formation of fear memories.
2022-07-19 | GSE199887 | GEO
Project description:Understanding the mechanisms by which long-term memories are formed and stored in the brain represents a central aim of neuroscience. Prevailing theory suggests that long-term memory encoding involves early plasticity within hippocampal circuits, while reorganization of the neocortex is thought to occur weeks to months later to subserve remote memory storage. Here we report that long-term memory encoding can elicit early transcriptional, structural and functional remodeling of the neocortex. Parallel studies using genome-wide RNA-sequencing, ultrastructural imaging, and whole-cell recording in wild-type mice suggest that contextual fear conditioning initiates a transcriptional program in the medial prefrontal cortex (mPFC) that is accompanied by rapid expansion of the synaptic active zone and postsynaptic density, enhanced dendritic spine plasticity, and increased synaptic efficacy. To address the real-time contribution of the mPFC to long-term memory encoding, we performed temporally precise optogenetic inhibition of excitatory mPFC neurons during contextual fear conditioning. Using this approach, we found that real-time inhibition of the mPFC inhibited activation of the entorhinal-hippocampal circuit and impaired the formation of long-term associative memory. These findings suggest that encoding of long-term episodic memory is associated with early remodeling of neocortical circuits, identify the prefrontal cortex as a critical regulator of encoding-induced hippocampal activation and long-term memory formation, and have important implications for understanding memory processing in healthy and diseased brain states. 4 biological replicates per group were analyzed. The material analyzed was medial prefrontal cortex (mPFC; anterior cingulate cortex subregion) from both brain hemispheres, from which total RNA was extracted.
2014-06-16 | E-GEOD-58510 | biostudies-arrayexpress