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Early-life antibiotic-driven dysbiosis in mice is associated with impaired metabolism and immunity in later life and reduced lifespan.

ABSTRACT: Early-life antibiotic-driven dysbiosis in mice is associated with impaired metabolism and immunity in later life and reduced lifespan.

PROVIDER: PRJNA646387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12225105_1.fastq.gz	Fastqsanger.gz
	SRR12225105_2.fastq.gz	Fastqsanger.gz
	SRR12225106_1.fastq.gz	Fastqsanger.gz
	SRR12225106_2.fastq.gz	Fastqsanger.gz
	SRR12225107_1.fastq.gz	Fastqsanger.gz

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Early-life antibiotic-driven dysbiosis in mice is associated with impaired metabolism and immunity in later life and reduced lifespan.

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Transcriptional memory of dFOXO activation in youth curtails later-life mortality

Project description:Identifying processes occurring in early life affect subsequent life and health span is an urgent aim to improve human health. In this study, we identified a novel mechanism of dFOXO in longevity determination in Drosophila. We found that early adulthood induction of dFOXO is sufficient to reduce mortality in old age through different pathways than chronic dFOXO. We showed that dFOXO requires specific ATP-dependent chromatin modifiers to extend lifespan, and we could mimic this lifespan extension by modulating dFOXO’s targets in later life. Furthermore, dFOXO in early life induces a specific transcriptional programme that counteracts the natural transcriptomic changes occurring with age. Our findings provide a better understanding of transcriptional mechanisms related to longevity and opens new avenues for possible time-restricted interventions to improve human health in the future.

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Chd8 haploinsufficiency impairs early brain development and impacts protein homeostasis later in life

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Lifespan Socioeconomic Context: Associations With Cognitive Functioning in Later Life.

Project description:ObjectivesEarly socioeconomic status (SES) correlates with later-life cognition. However, the effect of socioeconomic context (SEC), which reflects influences from broader ecological contexts, has not been examined. The present study developed a measure of SEC using lifetime residential addresses and examined SEC and residential mobility effects on later-life cognition.MethodOlder adults (N = 117, Mage = 75) reported addresses since birth. Latent SEC was constructed from census income, employment, and education (1920-2010) for each county and census year, extrapolated between census years. Controlling for current SES, SEC in childhood (ages 0-18) and adulthood (ages 19-60), with finer granulations in young adulthood (ages 19-39) and midlife (ages 40-60), predicted later-life cognition. Effects of residential mobility on later-life cognition were also examined.ResultsHigher childhood and adulthood SEC were associated with better Auditory Verbal Learning Test recognition (β = .24, p = .012) and immediate recall (β = .26, p = .008). Higher midlife SEC was associated with faster task switching (β = .26, p = .025) and better task switching efficiency (β = .27, p = .022). Higher residential mobility in childhood was associated with higher crystallized intelligence (β = .194, p = .040).DiscussionIndependent of current SES, childhood and adulthood SEC predicted later-life cognition, which may be sensitive to effects of social institutions and environmental health. SEC assessed across the lifespan, and related residential mobility information may be important complements to SES in predicting later-life cognitive health.

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Project description:The causal relationships between insulin levels, insulin resistance, and longevity are not fully elucidated. Genetic down-regulation of insulin/insulin-like growth factor 1 (Igf1) signaling components can extend invertebrate and mammalian lifespan, but insulin resistance, a natural form of decreased insulin signaling, is associated with greater risk of age-related disease in mammals. We compared Ins2+/- mice to Ins2+/+ littermate controls, on a genetically stable Ins1-null background. Proteomic and transcriptomic analyses of livers from 25 week-old mice suggested potential for healthier aging and altered insulin sensitivity in Ins2+/- mice. Halving Ins2 lowered circulating insulin by 25-34% in aged female mice, without altering Igf1 or circulating Igf1. Remarkably, decreased insulin led to lower fasting glucose and improved insulin sensitivity in aged mice. Moreover, lowered insulin caused significant lifespan extension, observed across two diverse diets. Our study indicates that elevated insulin contributes to age-dependent insulin resistance, and that limiting basal insulin levels can extend lifespan.

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