Monday, December 11, 2017

Study using a Drosophila model of traumatic brain injury suggests link to mitochondrial activity

Sen A, Gurdziel K, Liu J, Qu W, Nuga OO, Burl RB, Hüttemann M, Pique-Regi R, Ruden DM. Smooth, an hnRNP-L Homolog, Might Decrease Mitochondrial Metabolism by Post-Transcriptional Regulation of Isocitrate Dehydrogenase (Idh) and Other Metabolic Genes in the Sub-Acute Phase of Traumatic Brain Injury. Front Genet. 2017 Nov 15;8:175. PMID: 29187863; PMCID: PMC5694756.

From the abstract: "Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. ... To investigate the underlying genetic and molecular basis of TBI, we subjected w1118 Drosophila melanogaster to mild closed head trauma and found that mitochondrial activity is reduced in the brains of these flies 24 h after inflicting trauma. To determine the transcriptomic changes after mild TBI, we collected fly heads 24 h after inflicting trauma, and performed RNA-seq analyses. ... Based on these results, we propose a model in which TBI temporarily decreases mitochondrial activity in the brain 24 h after inflicting trauma ... We further propose that decreasing metabolism after TBI in such a manner is a protective mechanism that gives the brain time to repair cellular damage induced by TBI."

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