Transgenerational effects of exercise on mouse brain and cognition
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA899092 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22221119.fastq.gz | Fastqsanger.gz | |||
| SRR22221120.fastq.gz | Fastqsanger.gz | |||
| SRR22221121.fastq.gz | Fastqsanger.gz | |||
| SRR22221122.fastq.gz | Fastqsanger.gz | |||
| SRR22221123.fastq.gz | Fastqsanger.gz |
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Project description:Lifestyle induces long lasting effects on the brain and cognition, with some interventions like stress including transgenerational inheritance on the next generations mediated by epigenetic mechanisms. Physical exercise is one potent intervention driving robust improvements of cognition and brain health, also inducing intergenerational transmission to the litter. However, little is known about whether exercise effects may be transgenerationally transmitted. Here we analyzed the adult hippocampal neurogenesis (AHN) and the behavioral phenotype of sedentary adult male mice of the F2 generation of exercised grandfathers (F0, patrilineal design). Both F1 and F2 were sedentary, while F0 performed a moderate exercise training. We found that the F2 mice from exercised F0 acquired and recalled both spatial and non-spatial information better than F2 from sedentary F0. Contextual fear conditioning resulted not affected, together with no differences in the AHN markers. These results demonstrate that the transgenerational transmission of the effects of exercise on specific cognitive tasks persists after two generations, even though some of the cellular changes induced in F1 disappear in F2, and suggest that moderate exercise training has a longer-lasting effect than previously thought, and this aspect is worth taking into account in public health programs.
2024-06-12 | GSE217487 | GEO
Project description:Intergenerational transmission of the positive effects of physical exercise on brain and cognition
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Project description:Physical exercise seems universally beneficial to human and animal health, slowing cognitive aging and neurodegeneration. Cognitive benefits are tied to increased plasticity and reduced inflammation within the hippocampus, yet little is known about the factors and mechanisms mediating these effects. We discovered “runner” plasma, collected from voluntarily running mice, infused into sedentary mice recapitulates the cellular and functional benefits of exercise on the adult brain. Importantly, runner plasma reduces baseline neuroinflammatory gene expression and experimentally induced brain inflammation. Plasma proteomic analysis revealed a striking increase in complement cascade inhibitors including clusterin (CLU), which is facilitating the anti-inflammatory effects of runner plasma. Intravenously injected CLU strongly binds to brain endothelial cells reducing their inflammatory gene expression in an acute model of brain inflammation and in Alzheimer’s disease model mice. Cognitively impaired patients participating in structured exercise for 6 months showed improved cognition and higher plasma clusterin levels. These findings demonstrate the existence of anti-inflammatory “exercise factors” that are transferrable, target the cerebrovasculature and benefit the brain, and are present in humans engaging in exercise.
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Project description:Parental moderate exercise induces positive effects on sedentary litter’s behavior, and on hippocampal gene expression, adult neurogenesis and mitochondrial activation
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Project description:Aging drives a progressive decline in cognition that may be delayed by exercise (Ex). Whether and how Ex induces changes in molecular and spatial signatures of aging across the brain remains little known. Herein, we assessed the effects of Ex against cognitive aging, and characterized the molecular and spatial changes by aging and upon Ex across the brain at the single-nuclei resolution. Overall, Ex demonstrated cognitive benefits in old mice and largely protected the brain cells against aging, especially the neurons. Ex regulated the inhibitory neuron-specific aging-associated genes Alcam, Cacna2d3, and Foxp2, and reorganized the spatial distribution of cells across the aging brain, which may collectively contribute to the rejuvenation of cognitive function in aged mice. This study provides invaluable insights into Ex-induced benefits against brain aging.
2025-05-01 | GSE271563 | GEO
Project description:Aging drives a progressive decline in cognition that may be delayed by exercise (Ex). Whether and how Ex induces changes in molecular and spatial signatures of aging across the brain remains little known. Herein, we assessed the effects of Ex against cognitive aging, and characterized the molecular and spatial changes by aging and upon Ex across the brain at the single-nuclei resolution. Overall, Ex demonstrated cognitive benefits in old mice and largely protected the brain cells against aging, especially the neurons. Ex regulated the inhibitory neuron-specific aging-associated genes Alcam, Cacna2d3, and Foxp2, and reorganized the spatial distribution of cells across the aging brain, which may collectively contribute to the rejuvenation of cognitive function in aged mice. This study provides invaluable insights into Ex-induced benefits against brain aging.
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Project description:Physical exercise seems universally beneficial to human and animal health, slowing cognitive aging and neurodegeneration. Cognitive benefits are tied to increased plasticity and reduced inflammation within the hippocampus, yet little is known about the factors and mechanisms mediating these effects. We discovered that “runner” plasma, collected from voluntarily running mice and infused into sedentary mice, reduces baseline neuroinflammatory gene expression and experimentally induced brain inflammation. Plasma proteomic analysis revealed a concerted increase in complement cascade inhibitors including clusterin (CLU), a central protein for the anti-inflammatory effects of runner plasma. Intravenously injected CLU strongly binds to brain endothelial cells reducing their inflammatory gene expression in an acute model of brain inflammation and in an Alzheimer’s disease mouse model. Cognitively impaired patients participating in structured exercise for 6 months had higher plasma clusterin levels. These findings demonstrate the existence of anti-inflammatory “exercise factors” that are transferrable, target the cerebrovasculature and benefit the brain, and are present in humans engaging in exercise.
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Project description:Exercise exerts a wide range of beneficial effects for healthy physiology. However, the mechanisms regulating an individual's motivation to engage in physical activity remain incompletely understood. An important factor stimulating the engagement in both competitive and recreational exercise is the motivating pleasure derived from prolonged physical activity, which is triggered by exercise induced neurochemical changes in the brain. Here, we report on the discovery of a gut brain connection in mice that enhances exercise performance by augmenting dopamine signalling during physical activity. We find that microbiome dependent production of endocannabinoid metabolites in the gut stimulates the activity of TRPV1 expressing sensory neurons and thereby elevates dopamine levels in the ventral striatum during exercise. Stimulation of this pathway improves running performance, whereas microbiome depletion, peripheral endocannabinoid receptor inhibition, ablation of spinal afferent neurons or dopamine blockade abrogate exercise capacity. These findings indicate that the rewarding properties of exercise are influenced by gut derived interoceptive circuits and provide a microbiome dependent explanation for interindividual variability in exercise performance. Our study also suggests that interoceptomimetic molecules that stimulate the transmission of gut derived signals to the brain may enhance the motivation for exercise.
2023-03-15 | MSV000091494 | MassIVE
Project description:Regular voluntary exercise has been shown to increase waste transport through the glymphatic system in mice. Here, we investigated the impact of physical exercise on both upstream and downstream brain waste clearance in healthy volunteers via noninvasive MR imaging. Glymphatic influx, evaluated using intravenous contrast-enhanced dynamic T1 mapping, increased significantly at the putamen after 12 weeks of chronic exercise using a cycle ergometer (P=.01). The meningeal lymphatic vessel size and flow, measured by intravenous contrast-enhanced black-blood imaging and IR-ALADDIN technique, increased significantly after chronic exercise (P=.008 and P=.002, respectively). Plasma proteomics revealed significant changes in inflammation-related and immune-related proteins (down-regulated: S100A8, S100A9, PSMA3, and DEFA1A3; up-regulated: J chain) after chronic exercise, which correlated with glymphatic influx or mLV flow (P<.05). Our results suggest that increased glymphatic and mLV flow may be the potential mechanism underlying the neuroprotective effects of exercise on cognition, highlighting the importance of long-term, regular exercise.
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Project description:This project aims to study the change of brain protein lactylation under treadmill exercise training
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