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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082-12_MASTER]

ABSTRACT: Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082-12_MASTER]

PROVIDER: PRJNA1100204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28677655_1.fastq.gz	Fastqsanger.gz
	SRR28677655_2.fastq.gz	Fastqsanger.gz
	SRR28677656_1.fastq.gz	Fastqsanger.gz
	SRR28677656_2.fastq.gz	Fastqsanger.gz
	SRR28677657_1.fastq.gz	Fastqsanger.gz

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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age

Project description:Senescence is a cellular state linked to aging and age-onset disease across many mammalian species. Acutely, senescent cells promote wound healing and prevent tumor formation; but they are also pro-inflammatory, thus chronically exacerbate tissue decline. While senescent cells are active targets for anti-aging therapy, why these cells form in vivo, how they affect tissue aging, and the impact of their elimination remain unclear. Here we identify naturally-occurring senescent glia in aged Drosophila brains and decipher their origin and influence. Using AP1 activity to screen for senescence, we determine that senescent glia can appear in response to neuronal mitochondrial dysfunction. In turn, senescent glia promote lipid accumulation in non-senescent glia; similar effects are seen in senescent human fibroblasts in culture. Targeting AP1 activity in senescent glia mitigates senescence biomarkers, extends fly life and health span, and prevents lipid accumulation. However, these benefits come at the cost of increased oxidative damage in the brain, and neuronal mitochondrial function remains poor. Altogether, our results map the trajectory of naturally-occurring senescent glia in vivo and indicate that these cells link key aging phenomena: mitochondrial dysfunction and lipid accumulation.

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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082_28_MASTER]

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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082-12_MASTER]

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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082R-38_MASTER]

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Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age

| PRJNA1100203 | ENA

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082_28_MASTER]

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082_28_MASTER]

| PRJNA1100202 | ENA

Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082R-38_MASTER]

Project description:Senescent glia link neuronal mitochondrial dysfunction and lipid droplet accumulation with age [19082R-38_MASTER]

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The Glia-Neuron Lactate Shuttle and Elevated ROS Promote Lipid Synthesis in Neurons and Lipid Droplet Accumulation in Glia via APOE/D.

Project description:Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to glia, where they form lipid droplets (LDs). We show that glial and neuronal monocarboxylate transporters (MCTs), fatty acid transport proteins (FATPs), and apolipoproteins are critical for glial LD formation. MCTs enable glia to secrete and neurons to absorb lactate, which is converted to pyruvate and acetyl-CoA in neurons. Lactate metabolites provide a substrate for synthesis of fatty acids, which are processed and transferred to glia by FATP and apolipoproteins. In the presence of high ROS, inhibiting lactate transfer or lowering FATP or apolipoprotein levels decreases glial LD accumulation in flies and in primary mouse glial-neuronal cultures. We show that human APOE can substitute for a fly glial apolipoprotein and that APOE4, an Alzheimer's disease susceptibility allele, is impaired in lipid transport and promotes neurodegeneration, providing insights into disease mechanisms.

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