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BAG3 in traumatic brain injury: A cell-type-specific modulator of tau hyperphosphorylation.
Neural Regen Res
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Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, OH, USA (Sweeney N, Kim TY, Fu H).
Neuronal BAG3 attenuates tau hyperphosphorylation, synaptic dysfunction, and cognitive deficits induced by traumatic brain injury via the regulation of autophagy-lysosome pathway.
Acta Neuropathol
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Department of Neuroscience, College of Medicine, Ohio State University, Columbus, OH, USA.
Article Synopsis
- Early to mid-life traumatic brain injury (TBI) has been identified as a potential risk factor for developing Alzheimer's disease (AD) and related dementia.
- The study indicates that TBI reduces the expression of BCL2-associated athanogene 3 (BAG3), leading to a chain reaction of cognitive deficits and pathological changes in mice, including hyperphosphorylated tau accumulation and synaptic dysfunction.
- Overexpressing BAG3 specifically in neurons mitigated these AD-like symptoms, suggesting that targeting BAG3 could be a promising therapeutic approach to address TBI-induced cognitive decline.
Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice.
Front Neurosci
December 2017
Department of Anesthesiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Neuronal degeneration following traumatic brain injury (TBI) leads to intracellular accumulation of dysfunctional proteins and organelles. Autophagy may serve to facilitate degradation to overcome protein debris load and therefore be an important pro-survival factor. On the contrary, clearing may serve as pro-death factor by removal of essential or required proteins involved in pro-survival cascades.
View Article and Find Full Text PDFStress-response pathways are altered in the hippocampus of chronic alcoholics.
Alcohol
November 2013
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
The chronic high-level alcohol consumption seen in alcoholism leads to dramatic effects on the hippocampus, including decreased white matter, loss of oligodendrocytes and other glial cells, and inhibition of neurogenesis. Examining gene expression in post mortem hippocampal tissue from 20 alcoholics and 19 controls allowed us to detect differentially expressed genes that may play a role in the risk for alcoholism or whose expression is modified by chronic consumption of alcohol. We identified 639 named genes whose expression significantly differed between alcoholics and controls at a False Discovery Rate (FDR) ≤ 0.
View Article and Find Full Text PDFNear-infrared photobiomodulation in an animal model of traumatic brain injury: improvements at the behavioral and biochemical levels.
Photomed Laser Surg
September 2012
Department of Neurology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Objective: The purpose of this was to evaluate the neuroprotective effects of near-infrared (NIR) light using an in-vivo rodent model of traumatic brain injury (TBI), controlled cortical impact (CCI), and to characterize changes at the behavioral and biochemical levels.
Background Data: NIR upregulates mitochondrial function, and decreases oxidative stress. Mitochondrial oxidative stress and apoptosis are important in TBI.