Early Stem Cell Aging in the Mature Brain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA705899 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13826200_1.fastq.gz | Fastqsanger.gz | |||
| SRR13826200_2.fastq.gz | Fastqsanger.gz | |||
| SRR13826201_1.fastq.gz | Fastqsanger.gz | |||
| SRR13826201_2.fastq.gz | Fastqsanger.gz | |||
| SRR13826202_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 178 |
Similar Datasets
Project description:Stem cell dysfunction drives many age-related disorders. Identifying mechanisms that initially compromise stem cell behavior represent early targets to enhance stem cell function later in life. Here, we pinpoint multiple factors that disrupt neural stem cell (NSC) behavior in the adult hippocampus. Clonal tracing showed that NSCs exhibit asynchronous depletion by identifying short-term (ST-NSC) and long-term NSCs (LT-NSCs). ST-NSC divide rapidly to generate neurons and deplete in the young brain. Meanwhile, multipotent LT-NSCs are maintained for months, but are pushed out of homeostasis by lengthening quiescence. Single cell transcriptome analysis of deep NSC quiescence revealed several hallmarks of molecular aging in the mature brain and identified tyrosine-protein kinase Abl1 as an NSC pro-aging factor. Treatment with the Abl-inhibitor Imatinib increased NSC proliferation without impairing NSC maintenance in the middle-aged brain. Our study indicates that hippocampal NSCs are particularly vulnerable to cellular aging, yet NSC function can be partially restored.
2021-03-03 | GSE168031 | GEO
Project description:Stem cell dysfunction drives many age-related disorders. Identifying mechanisms that initially compromise stem cell behavior represent early targets to promote tissue function later in life. Here, we pinpoint multiple factors that disrupt neural stem cell (NSC) behavior in the adult hippocampus. Clonal tracing showed that NSCs exhibit asynchronous depletion by identifying short-term NSCs (ST-NSCs) and long-term NSCs (LT-NSCs). ST-NSCs divide rapidly to generate neurons and deplete in the young brain. Meanwhile, multipotent LT-NSCs are maintained for months but are pushed out of homeostasis by lengthening quiescence. Single-cell transcriptome analysis of deep NSC quiescence revealed several hallmarks of molecular aging in the mature brain and identified tyrosine-protein kinase Abl1 as an NSC aging factor. Treatment with the Abl inhibitor imatinib increased NSC activation without impairing NSC maintenance in the middle-aged brain. Our study indicates that hippocampal NSCs are particularly vulnerable and adaptable to cellular aging.
| S-EPMC10069280 | biostudies-literature
Project description:(Phospho)proteomic studies in the human aging brain are based on the comparison between controls of bain aging usually affected by early stages of neurofibrillary tangle (NFT) pathology and subjects with moderate or advanced Alzheimer’s disease (AD).
(Phospho)proteomics using conventional label‐free‐ and SWATH‐MS (Sequential window acquisition of all theoretical fragment ion spectra mass spectrometry) has been assessed in the frontal cortex (FC) of individuals without NFTs and SPs, and comorbidities classified by age (years) in four groups; group 1 (young, 30-44); group 2 (middle-aged: MA, 45-52); group 3 (early-elderly, 64-70); and group 4 (late-elderly, 75-85).
2023-08-11 | PXD035997 | JPOST Repository
Project description:This study investigates the proteomic alterations in brain mitochondria isolated from 5- (mature), 12- (old), and 24-month-old (aged) mice to examine normal "healthy" aging. Using quantitative mass-spectrometry based super-SILAC, our findings revealed global proteomic changes in brain mitochondria identifying several metabolic pathways including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. Overall, we found that the bioenergetic function of these mitochondria was preserved suggesting the proteomic alterations potentially allow for compensatory mechanisms to combat aging.
2015-01-27 | PXD001370 | Pride
Project description:The mammalian brain relies on neurochemistry to fulfill its functions. Yet, the complexity of the brain metabolome and its changes during diseases or aging remains poorly understood. To start bridging this gap, we generated a metabolome atlas of the aging mouse brain from 10 anatomical regions spanning from adolescence to late adulthood. We combined data from three chromatography-based mass spectrometry assays and structurally annotated 1,709 metabolites to reveal the underlying architecture of aging-induced changes in the brain metabolome. Overall differences between sexes were minimal. We found 94% of all metabolites to significantly differ between brain sections in at least one age group. We also discovered that 90% of the metabolome showed significant changes with respect to age groups. For example, we identified a shift in sphingolipid patterns during aging that is related to myelin remodeling in the transition from adolescent to adult brains. This shift was accompanied by large changes in overall signature in a range of other metabolic pathways. We found clear metabolic similarities in brain sections that were functionally related such as brain stem, cerebrum and cerebellum. In cerebrum, metabolic correlation patterns got markedly weaker in the transition from adolescent to ear adults, whereas correlation patterns between cerebrum and brainstem regions decreased from early to late adulthood. We were also able to map metabolic changes to gene and protein brain atlases to link molecular changes to metabolic brain phenotypes. Metabolic profiles can be investigated via https://atlas.metabolomics.us/. This new resource enables brain researchers to link new metabolomic studies to a foundation data set.
2020-12-23 | ST001637 | MetabolomicsWorkbench
Project description:In this study, gene expression of brain from postnatal (day 5) and aging (week 70) mice (C57BL/6J) was profiled. The data was used to infer transcriptional network of genes associated with epigenetic clock and GnRHR pathway in the brain. The results of this study suggested that brain aging originated early-in life.
2022-10-12 | GSE215138 | GEO
Project description:Here we show that the aging of neural stem and progenitor cells (NSPCs) in the mouse brain is characterized by a decrease in the generation efficacy of proliferative NSPCs, rather than the changes in lineage specificity of NSPCs. We reveal that the downregulation of age-dependent genes in NSPCs drives cell aging by decreasing the population of actively proliferating NSPCs, while increasing the expression of quiescence markers. We find that epigenetic deregulation of MLL complex at promoters leads to transcriptional inactivation of age-dependent genes, highlighting the importance of the dynamic interaction between histone modifiers and gene regulatory elements in regulating transcriptional program of aging cells. Our study sheds light on the key intrinsic mechanisms driving stem cell aging through epigenetic regulators and identifies potential rejuvenation targets that could restore the function of aging stem cells.
2023-11-02 | GSE212725 | GEO
Project description:MicroRNAs (miRNAs) are endogenous small RNA molecules that regulate gene expression post-transcriptionally. Work in Caenorhabditis elegans has shown that specific miRNAs function in lifespan regulation and in a variety of age-associated pathways, but the roles of miRNAs in the aging of vertebrates are not well understood. We examined the expression of small RNAs in whole brains of young and old mice by deep sequencing and report here on the expression of 233 known miRNAs and identification of 41 novel miRNAs. Of these miRNAs, 75 known and 18 novel miRNAs exhibit greater than 2.0-fold expression changes. The majority of expressed miRNAs in our study decline in relative abundance in the aged brain, in agreement with trends observed in other miRNA studies in aging tissues and organisms. Target prediction analysis suggests that many of our novel aging-associated miRNAs target genes in the insulin signaling pathway, a central node of aging-associated genetic networks. These novel miRNAs may thereby regulate aging-related functions in the brain. Since mouse miRNAs are conserved in humans, the aging-affected brain miRNAs we report here may represent novel regulatory genes that function during aging in the human brain. 2 samples examined: Mouse brain from two young (5 months) and two old animals (24-25 months).
2012-05-31 | E-GEOD-34393 | biostudies-arrayexpress
Project description:RNA-seq was performed to identify genetic contributors to barrier phenotype. Brain endothelial cell-like cells derived from human induced pluripotent stem cells (hiPSC-BEC-like cells) were differentiated in the presence of barrier enhancing molecules like retinoic acid (RA) and retinoid X receptor agonist (CD3254) or DMSO as a vehicle control to yield hiPSC-BEC-like cells that display mature and immature barrier properties respectively. RNA was isolated from 3 independent differentiations and sequenced to identify differentially expressed genes in the mature versus immature conditions.
2023-03-10 | E-MTAB-12678 | biostudies-arrayexpress