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Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

ABSTRACT: Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

PROVIDER: PRJNA725513 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14334200_1.fastq.gz	Fastqsanger.gz
	SRR14334200_2.fastq.gz	Fastqsanger.gz
	SRR14334201_1.fastq.gz	Fastqsanger.gz
	SRR14334201_2.fastq.gz	Fastqsanger.gz
	SRR14334202_1.fastq.gz	Fastqsanger.gz

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Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

Project description:Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

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Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

Project description:Reducing mitochondrial electron transport induces a Warburg-like shift to accommodate for the energetic burden caused by brain trauma and salvage dopaminergic neurons. This metabolic shift is evident in the transcriptional upregulation of key genes in the Pyruvate Dehydrogenase Complex and glycolytic pathway.

2021-08-26 | GSE173431 | GEO

Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

Project description:Reducing mitochondrial electron transport induces a Warburg-like shift to accommodate for the energetic burden caused by brain trauma without overwhelming mitochondrial cellular respiration and cellular redox to salvage dopaminergic neurons. This metabolic shift is evident in the transcriptional upregulation of key genes in the Pyruvate Dehydrogenase Complex and glycolytic pathway.

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Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration.

Project description:Concussion is associated with a myriad of deleterious immediate and long-term consequences. Yet the molecular mechanisms and genetic targets promoting the selective vulnerability of different neural subtypes to dysfunction and degeneration remain unclear. Translating experimental models of blunt force trauma in C. elegans to concussion in mice, we identify a conserved neuroprotective mechanism in which reduction of mitochondrial electron flux through complex IV suppresses trauma-induced degeneration of the highly vulnerable dopaminergic neurons. Reducing cytochrome C oxidase function elevates mitochondrial-derived reactive oxygen species, which signal through the cytosolic hypoxia inducing transcription factor, Hif1a, to promote hyperphosphorylation and inactivation of the pyruvate dehydrogenase, PDHE1α. This critical enzyme initiates the Warburg shunt, which drives energetic reallocation from mitochondrial respiration to astrocyte-mediated glycolysis in a neuroprotective manner. These studies demonstrate a conserved process in which glycolytic preconditioning suppresses Parkinson-like hypersensitivity of dopaminergic neurons to trauma-induced degeneration via redox signaling and the Warburg effect.

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Adverse Impact of Female Reproductive Signaling on Age-Dependent Neurodegeneration After Mild Head Trauma in Drosophila

Project description:Environmental insults, including mild head trauma, significantly increase the risk of neurodegeneration. However, it remains challenging to establish a causative connection between early-life exposure to mild head trauma and late-life emergence of neurodegenerative deficits, nor do we know how sex and age compound the outcome. Using aDrosophilamodel, we demonstrate that exposure to mild head trauma causes neurodegenerative conditions that emerge late in life and disproportionately affect females. Increasing age-at-injury further exacerbates this effect in a sexually dimorphic manner. We further identify Sex Peptide (SP) signaling as a key factor in female susceptibility to post-injury brain deficits. RNA sequencing highlights changes in innate immune defense transcripts specifically in mated females during late life. Our findings establish a causal relationship between early head trauma and late-life neurodegeneration, emphasizing sex differences in injury response and the impact of age-at-injury. Finally, our findings reveal that reproductive signaling adversely impacts female response to mild head insults and elevates vulnerability to late-life neurodegeneration.

2024-08-29 | GSE274136 | GEO

TREM2 shapes myeloid cell activations in trauma- and autoimmune-mediated neurodegeneration

Project description:TREM2 signaling in myeloid cells functions as a major pathology-induced immune signaling hub in trauma- and autoimmune-mediated neurodegeneration. Here we compared the influence of TREM2 signaling on single-cell transcriptional profiles of mouse myeloid populations during the pathologies of spinal cord injury (SCI) and multiple sclerosis (MS) models.

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Project description:Purpose: The purpose of this study was to examine the effect blast preconditioning on the structure and function of retinal ganglion cells (RGC), and to identify molecular pathways that contribute to RGC loss. Methods: To examine the effect of blast-preconditioning three groups of mice were analyzed, including those 1) subjected to sham injury followed by one single 20 PSI injury one week later, 2) mice exposed to two low intensity preconditioning blast exposures separated by one week (5 PSI, 5 PSI) and 3) mice exposed to a preconditioning injury (5 PSI) followed by a single 20 PSI blast exposure one week later. RNAseq analysis was used to identify transcriptional changes between groups. Conclusions: Preconditioning protects RGC from blast injury. Protective effects appear to involve changes in kynurenine-3-monooxygenase activity, whose inhibition is also protective.

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Genomics of preconditioning

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