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Longitudinal tracking of whole blood gene-expression in healthy young and old individuals - 2014

ABSTRACT: Immune responses generally decline with age. We used multiple ‘omics’ technologies to capture population- and individual- level changes in the human immune system of 135 healthy adult individuals of different ages sampled longitudinally over a nine-year period. We observe a high inter-individual variability in the rates of change of cellular frequencies that correlate with baseline values, allowing identification of steady state levels towards which a cell subset converges and the ordered convergence of multiple cell subsets towards an older adult homeostasis. These form a high dimensional trajectory of immune-aging (IMM-AGE) that describes a person’s immune status better than chronological age. We show the IMM-AGE score predicts all-cause mortality beyond well-established risk factors in the Framingham Heart Study.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123697 | GEO | 2018/12/13

REPOSITORIES: GEO

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Project description:Physical exercise stimulates adult hippocampal neurogenesis in mammals, and is considered a relevant strategy for preventing age-related cognitive decline in aging humans. However, its mechanism is controversial. Here, by investigating microRNAs (miRNAs) and their downstream pathways, we uncover that downregulation of miR-135a-5p mediates exercise-induced proliferation of adult NPCs in adult neurogenesis in the mouse hippocampus, likely by activation of phosphatidylinositol (IP3) signaling. Specifically, while overexpression of miR-135 prevents exercise-induced proliferation in the adult mouse hippocampus in vivo and in NPCs in vitro, its inhibition activates NPCs proliferation in resting and aged mice. Label free proteomics and bioinformatics analysis identifies 11 potential targets of miR-135 in NPCs, several of them involved in phosphatidylinositol signaling. Thus, miR-135a is key in mediating exercise-induced adult neurogenesis and opens intriguing perspectives toward the therapeutic exploitation of miR-135 to delay or prevent pathological brain ageing.Physical exercise stimulates adult hippocampal neurogenesis in mammals, and is considered a relevant strategy for preventing age-related cognitive decline in aging humans. However, its mechanism is controversial. Here, by investigating microRNAs (miRNAs) and their downstream pathways, we uncover that downregulation of miR-135a-5p mediates exercise-induced proliferation of adult NPCs in adult neurogenesis in the mouse hippocampus, likely by activation of phosphatidylinositol (IP3) signaling. Specifically, while overexpression of miR-135 prevents exercise-induced proliferation in the adult mouse hippocampus in vivo and in NPCs in vitro, its inhibition activates NPCs proliferation in resting and aged mice. Label free proteomics and bioinformatics analysis identifies 11 potential targets of miR-135 in NPCs, several of them involved in phosphatidylinositol signaling. Thus, miR-135a is key in mediating exercise-induced adult neurogenesis and opens intriguing perspectives toward the therapeutic exploitation of miR-135 to delay or prevent pathological brain ageing.

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Longitudinal tracking of whole blood gene-expression in healthy young and old individuals - 2014

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