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Molecular signatures of immune cells and neuroblasts in the aged brain

ABSTRACT: Normal aging is accompanied by escalating systemic inflammation. To comprehensively characterize the impact of aging on immune cells in the brain and periphery, we harvested immune cells from mouse spleen and brain tissues. Single cell sequencing was performed to compare the genetic signatures in these isolated immune cell subsets from spleen and brain tissues in young and aged mice. Our results demonstrate increased accumulations of immune cells such as natural killer (NK) cells in the aged brain as compared to the young brain. In addition, NK cells in the aged brain display augmented proliferation activity and cytotoxicity. RNA-sequencing of neuroblasts isolated from the aged brain revealed that aging induces dysregulated expression of genes related to DNA damage response and upregulation of senescence signatures.

ORGANISM(S): Mus musculus

PROVIDER: GSE157771 | GEO | 2020/09/11

REPOSITORIES: GEO

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Molecular signatures of immune cells and neuroblasts in the aged brain

Project description:Normal aging is accompanied by escalating systemic inflammation. To comprehensively characterize the impact of aging on immune cells in the brain and periphery, we harvested immune cells from mouse spleen and brain tissues. Single cell sequencing was performed to compare the genetic signatures in these isolated immune cell subsets from spleen and brain tissues in young and aged mice. Our results demonstrate increased accumulations of immune cells such as natural killer (NK) cells in the aged brain as compared to the young brain. In addition, NK cells in the aged brain display augmented proliferation activity and cytotoxicity. RNA-sequencing of neuroblasts isolated from the aged brain revealed that aging induces dysregulated expression of genes related to DNA damage response and upregulation of senescence signatures.

2020-09-11 | GSE157770 | GEO

The effects of aging vs. alpha7 nAChR subunit deficiency on the mouse brain transcriptome

Project description:Aging is accompanied by expression changes in multiple genes and the brain is one of the tissues most vulnerable to aging. Since the alpha7 nicotinic acetylcholine receptor (nAChR) subunit has been associated with neurodevelopmental disorders and cognitive decline during aging, we hypothesized that its absence might affect gene expression profiles in aged brains. To study whether transcriptional changes occur due to aging, alpha7 deficiency or both, we analyzed whole brain transcriptomes of young (8 week) and aged (2 year) alpha7 deficient and wild-type control mice, using Mouse Genome 430 2.0 microarray. Highly significant expression changes were detected in 47 and 1543 genes (after Bonferroni and FDR correction) in the brains of aged mice compared to young mice, regardless of their genotype. These included genes involved in immune system function and ribosome structure, as well as genes that were previously demonstrated as differentially expressed in aging human brains. Genotype-dependent changes were detected in only 3 genes, Chrna7 which encodes the alpha7 nAChR subunit, and two closely linked genes, likely due to a mouse background effect. Expression changes dependent on age-genotype interaction were detected in 207 genes (with a low significance threshold). Age-dependent differential expression levels were approved in all nine genes that were chosen for validation by real-time RT-PCR. Our results suggest that the robust effect of aging on brain transcription clearly overcomes the almost negligible effect of alpha7 nAChR subunit deletion, and that germline deficiency of this subunit has a minor effect on brain expression profile in aged mice. Total of 20 samples. 10 from young adult mice (8 weeks) and 10 from aged mice (2 years). In each age group, 5 were wild-type control mice and 5 alpha7 nAChR subunit defecient mice

2011-01-01 | E-GEOD-20411 | biostudies-arrayexpress

Young blood-derived platelet factors abate inflammation and rescue recognition in aging.

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.

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Global quantitative proteomics of mouse brain structures reveals significant alterations in expression of proteins involved in neuronal plasticity during aging

Project description:Aging is believed to be the result of alterations of protein expression and accumulation of changes in biomolecules. Although there are numerous reports demonstrating changes in protein expression in brain during aging, only few of them describe global changes in the protein level. Here, we present a deepest quantitative proteomic analysis of three brain regions, hippocampus, cortex and cerebellum, in mice aged 1 and 12 months, using the total protein approach technique. In all the brain regions, both in young and in middle-aged animals, we identified over 6,700 proteins. We found that although the total protein expression in middle-aged brain structures is practically unaffected by aging, there are significant differences between young adult and middle-aged mice in the expression of some receptors and signaling cascade proteins proven to be significant for learning and memory formation. Our analysis demonstrates that hippocampus is the most unstable structure during natural aging and that the first symptoms of weakening of neuronal plasticity may be observed on protein level in middle-aged animals.

2018-07-03 | PXD009792 | Pride

Young bone marrows transplantation rejuvenates immune cells, attenuate cerebral Aβ accumulation and related pathologies in Alzheimer’s disease model mouse

Project description:Immunesenescence contributes to systematic aging and participates in the pathogenesis of Alzheimer’s disease (AD). To define the potential of immune rejuvenation in AD therapy, we reconstituted the immune systems of aged APP/PS1 mice through bone marrow transplantation (BMT). Single cell RNA sequencing (ScRNA-seq) of peripheral blood mononuclear cells (PBMCs) indicated that young BMT reverse the expression of aging- and AD-related genes in multiple cell types of PBMCs. Plasma proteome profiling also indicated the reduction of the plasma level of senescence-associated secretory phenotype (SASP) proteins after young BMT. Young BMT significantly reduced central and peripheral Aβ levels, alleviated brain Aβ plaque burden, neuronal degeneration, neuroinflammation, and behavioral deficits in the aged APP/PS1 mice. These effects occurred with the improved Aβ capacity of peripheral monocytes. Collectively, our study demonstrated that rejuvenation of immune system could decrease brain Aβ deposition and other AD-type pathologies, representing a potential therapeutic approach for AD.

2023-06-27 | GSE235527 | GEO