Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1122961 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29367574_1.fastq.gz | Fastqsanger.gz | |||
| SRR29367574_2.fastq.gz | Fastqsanger.gz | |||
| SRR29367575_1.fastq.gz | Fastqsanger.gz | |||
| SRR29367575_2.fastq.gz | Fastqsanger.gz | |||
| SRR29367576_1.fastq.gz | Fastqsanger.gz |
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Project description:Environmental enrichment has been reported to delay or restore age-related cognitive deficits, however, a mechanism to account for the cause and progression of normal cognitive decline and its preservation by environmental enrichment is lacking. Using genome-wide SAGE-Seq, we provide a global assessment of differentially expressed genes altered with age and environmental enrichment in the hippocampus. Qualitative and quantitative proteomics in naïve young and aged mice was used to further identify phosphorylated proteins differentially expressed with age. We found that increased expression of endogenous protein phosphatase-1 inhibitors in aged mice may be characteristic of long-term environmental enrichment and improved cognitive status. As such, hippocampus-dependent performances in spatial, recognition, and associative memories, which are sensitive to aging, were preserved by environmental enrichment and accompanied by decreased protein phosphatase activity. Age-associated phosphorylated proteins were also found to correspond to the functional categories of age-associated genes identified through transcriptome analysis. Together, this study provides a comprehensive map of the transcriptome and proteome in the aging brain, and elucidates endogenous protein phosphatase-1 inhibition as a potential means through which environmental enrichment may ameliorate age-related cognitive deficits. 4 groups with 3 biological replicates per group: aged in environmental enrichment (EA), aged in standard housing (SA), young in environmental enrichment (EY), and young in standard housing (SY).
2015-06-24 | E-GEOD-43718 | biostudies-arrayexpress
Project description:There is a progressive decline in physiological function with age, and aging is associated with increased susceptibility to injury and infection. However, several reports have indicated that the agility of youth is characterized by transferable rejuvenating molecular factors, as was observed previously in heterochronic parabiosis experiments. These experiments demonstrated a rejuvenating effect of young blood in old animals. There have been several efforts to characterize these youthful or maturation-associated factors in the young blood. In this report, we demonstrate the resilience of young mice, at or before puberty, to polymicrobial sepsis and show an age-dependent effect of plasma extracellular vesicles on the outcome following sepsis. The EVs from the young mice were cytoprotective, anti-inflammatory, and reduced cellular senescence markers. MicroRNA sequencing of the extracellular vesicles showed an age-associated signature and identified miR-296-5p and miR-541-5p to progressively reduce their levels in the blood plasma with increasing age. We further show that the levels of these miRNAs decline with age in multiple organs. The miRNAs miR-296-5p and miR-541-5p showed a reparatory effect in an in vitro wound healing model and the miR-296-5p, when given intraperitoneally, reduced mortality in the mouse model of sepsis. In summary, our studies demonstrate that EVs from very young mice have a reparative effect on sepsis, and the reparative factors are likely maturation-dependent. Our observation that miR-296-5p and miR-541-5p are plasma EV constituents that significantly reduce with age and can reduce inflammation suggests a therapeutic potential for these miRNAs in inflammation and age-associated diseases.
2025-06-30 | GSE300900 | GEO
Project description:Background: Age-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption’s well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep’s relationship to cognitive aging. Methodology: We measured sleep stages in young adult and aged F344 rats during inactive (enhanced sleep) and active (enhanced wake) periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken. Principal Findings: Water maze performance was impaired, and inactive period deep sleep was decreased with age. However, increased deep sleep during the active period was most strongly correlated to maze performance. Transcriptional profiles were strongly associated with behavior and age, and were validated against prior studies. Bioinformatic analysis revealed increased translation and decreased myelin/ neuronal pathways. Conclusions: The F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep. Microarray analysis suggests that the processes engaged by this sleep are consistent with its function. Thus, active period deep sleep appears temporally misaligned but mechanistically intact, leading to the following: first, aged brain tissue appears capable of generating the slow waves necessary for deep sleep, albeit at a weaker intensity than in young. Second, this activity, presented during the active period, seems disruptive rather than beneficial to cognition. Third, this active period deep sleep may be a cognitively pathologic attempt to recover age-related loss of inactive period deep sleep. Finally, therapeutic strategies aimed at reducing active period deep sleep (e.g., by promoting active period wakefulness and/or inactive period deep sleep) may be highly relevant to cognitive function in the aging community. KEYWORDS: frontal cortex, rat, young or aged We implanted young and aged Fischer 344 rats (n = 6/ group) with wireless EEG, EMG and movement monitoring devices to measure sleep architecture. Animals were trained in the Morris water maze to assess cognitive function, and frontal cortices were removed for microarray analysis.sleep disruption and cognitive decline.
2011-04-21 | E-GEOD-24515 | biostudies-arrayexpress
Project description:This study focused on transcription in the medial PFC (mPFC) as a function of age and cognition. Young and aged F344 rats were characterized on tasks, attentional set shift and spatial memory, which depend on the mPFC and hippocampus, respectively. Differences in transcription associated with age and cognitive function were examined using RNA sequencing to construct transcriptomic profiles for the mPFC, white matter, and region CA1 of the hippocampus. The results indicate regional differences in vulnerability to aging associated with increased expression of immune and defense response genes and a decline in synaptic and neural activity genes. Importantly, we provide evidence for region specific transcription related to behavior. In particular, expression of transcriptional regulators and neural activity-related immediate-early genes (IEGs) are increased in the mPFC of aged animals that exhibit delayed set shift behavior; relative to age-matched animals that exhibit set shift behavior similar to younger animals. The study contains 11 young and 20 aged rats for the mPFC and CA1 samples, which were used to investigate expression patterns associated with aging and behavior. White matter samples were used to investigate an age-related effect with 8 young and 9 aged rats.
2016-05-17 | E-GEOD-75772 | biostudies-arrayexpress
Project description:We show that platelet factors transfer rejuvenating effects of young plasma to the aging brain. Proteomic analysis of plasma from young and aged mice identified age-related changes in platelets. Systemic exposure of aged animals to the platelet fraction of young plasma decreased hippocampal neuroinflammation at a transcriptional and cellular level and ameliorated cognitive impairments. We identified the platelet-derived chemokine CXCL4/Platelet Factor-4 (PF4) as a pro-youthful circulating factor. Systemic PF4 administration decreased age-related neuroinflammation, restored the aging peripheral immune system to a more youthful state, and improved hippocampal-dependent learning and memory in aged mice.
2023-06-20 | GSE173254 | GEO
Project description:Changes in peripheral CD8+ T cells are a prominent hallmark of immune aging. While infiltrating CD8+ T cells are implicated in aging and neurodegenerative disease-related pathology in the brain, the role of aged non-infiltrating CD8+ T cells has yet to be fully defined. Here, we show that targeting activated aged peripheral CD8+ T cells rescues age-related cognitive decline. Using heterochronic parabiosis and single cell transcriptomics analysis we observed that aged peripheral CD8+ T cells maintain properties intrinsic to their age, being refractory to the effects of a young or aged systemic milieu. Systemic exposure of young mice to aged CD8+ T cells elicited synaptic-related aging transcriptional signatures in the hippocampus and impaired cognition. Inhibiting migration of aged peripheral CD8+ T cells to lymph nodes mitigated pro-aging effects on the young hippocampus. Conversely, targeting aged CD8+ T cells restored synaptic-related signatures in the aged hippocampus and ameliorated cognitive impairments. Mechanistically, we identified granzyme k (GZMK) as a secreted age-associated CD8+ T cell-derived factor that impairs cognitive function. Together, our data identify activated aged CD8+ T cells and their secreted factors as potential therapeutic targets to rescue cognition in old age.
2025-05-02 | GSE266468 | GEO
Project description:Changes in peripheral CD8+ T cells are a prominent hallmark of immune aging. While infiltrating CD8+ T cells are implicated in aging and neurodegenerative disease-related pathology in the brain, the role of aged non-infiltrating CD8+ T cells has yet to be fully defined. Here, we show that targeting activated aged peripheral CD8+ T cells rescues age-related cognitive decline. Using heterochronic parabiosis and single cell transcriptomics analysis we observed that aged peripheral CD8+ T cells maintain properties intrinsic to their age, being refractory to the effects of a young or aged systemic milieu. Systemic exposure of young mice to aged CD8+ T cells elicited synaptic-related aging transcriptional signatures in the hippocampus and impaired cognition. Inhibiting migration of aged peripheral CD8+ T cells to lymph nodes mitigated pro-aging effects on the young hippocampus. Conversely, targeting aged CD8+ T cells restored synaptic-related signatures in the aged hippocampus and ameliorated cognitive impairments. Mechanistically, we identified granzyme k (GZMK) as a secreted age-associated CD8+ T cell-derived factor that impairs cognitive function. Together, our data identify activated aged CD8+ T cells and their secreted factors as potential therapeutic targets to rescue cognition in old age.
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Project description:Repeated excessive alcohol consumption increases the risk of developing cognitive decline and dementia. Hazardous drinking among older adults further increases such vulnerabilities. In order to understand the molecular mechanisms underlying alcohol-induced cognitive deficits in older adults, we performed a chronic intermittent ethanol exposure paradigm (ethanol or water gavage every other day 10 times) in 8-week-old young adult and 70-week-old aged rats. While spatial memory retrieval ascertained by probe trials in the Morris water maze was not significantly different between ethanol-treated and water-treated rats in both age groups after the fifth and tenth gavages, behavioral flexibility was impaired in ethanol-treated rats than water-treated rats in the aged group but not in the young adult group. Further proteomic and phosphoproteomic analyses on their hippocampal tissues by tandem mass tag mass spectrometry revealed ethanol-treatment-associated proteomic and phosphoproteomic differences distinct to the aged rats, including the upregulations of Prkcd protein level, several of its phosphosites, and its kinase activity and the same aspects in Camk2a but downregulated, and were enriched in pathways involved in neurotransmission regulation, synaptic plasticity, neuronal apoptosis, and insulin receptor signaling. In conclusion, our behavioral and proteomic results added several candidate proteins and pathways potentially associated with alcohol-induced cognitive decline in aged adults.
2023-03-11 | PXD034443 | Pride
Project description:Young blood or plasma and young bone marrow improves cognitive function in aged animals, though the cell type responsible for these regenerative effects remains unknown. The current study used induced pluripotent stem cells (iPSCs) to assess the potential of mononuclear phagocytes as a therapeutic for age-associated cognitive decline, as iPSCs provide a source of autologous blood cells without the risk of immune rejection or graft vs. host disease. Human iPSCs differentiated into mononuclear phagocytes (iMPs) were administered to aging, genetically immunocompromised NOD scid gamma mice via tail vein injection. Aging mice receiving iMP treatment showed significant improvements in behavioral tasks relying on spatial working memory and on hippocampus-dependent short-term memory. iMP treatment also had significant effects on several key neural health markers. Expression of the synaptic transporter, VGLUT1, was decreased in untreated aging mice, and levels were restored in aging mice treated with iMPs. Aging mice also had increased numbers of astrocytes and microglia, as well as decreased microglial branching, which were all reversed by iMP treatment. Profiling of the plasma via proteomics and the hippocampus via single nuclei RNA sequencing identified several pathways that may mediate the effects of iMPs. snRNA-seq analysis also revealed that iMP treatment increased a subpopulation of hippocampal mossy cells in aging mice. iPSCs offer an autologous therapy and based on a range of benefits, iPSC-derived mononuclear phagocytes are a promising new therapeutic strategy for age-associated declines in cognition and neural health.
2025-09-10 | GSE220548 | GEO
Project description:The mechanisms underlying dementia, including Alzheimer’s Disease (AD), associated with aging remain elusive. Our RNA sequencing analysis (RNA-Seq) revealed that the loss of steroid receptor coactivator-1 (SRC-1) leads to alterations in gene expression signatures that are commonly associated with neurodegenerative diseases, including AD. Consistent with previous findings, our research indicates that SRC-1 deficiency diminishes the neural plasticity of the hippocampal CA1 neurons. Cognitive behavior tests demonstrate that both SRC-1-KO mice and mice with a humanized SRC-1 mutation (SRC-1L1376P) displayed early signs of contextual memory impairment at just 6 months of age, in contrast to the typical aging-associated memory decline observed in wild type mice at 18 months of age. These results suggest a protective role of SRC1 against aging-associated cognitive decline. To further explore the molecular mechanism, we reanalyzed publicly available spatial RNA-Seq data of both young and aged mouse brains. We found a synchronous decline in SRC-1 and S100 calcium-binding protein A6 (S100A6), an AD associated gene, in both the hypothalamus and hippocampus of aged brain. Notably, our RNA-Seq data highlighted S100A6 as one of the most profoundly inhibited genes in SRC-1-KO mice. We also identified S100A6 and S100A11 as potential AD-associated genes that are downstream targets of SRC-1, offering novel perspectives on the protective role of SRC1 against cognitive decline due to aging.
2025-09-17 | GSE278158 | GEO