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10.1177/1759091418781921 http://scihub22266oqcxt.onion/10.1177/1759091418781921 C6050992!6050992 !29932344     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29932344 &cmd=llinks): Failed to open stream: HTTP request failed! 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Repeated Mild Closed Head Injuries Induce Long-Term White Matter Pathology and Neuronal Loss That Are Correlated With Behavioral Deficits |pdf=|usr=}}{{29932344 }} gab.com Text Repeated Mild Closed Head Injuries Induce Long-Term White Matter Pathology and Neuronal Loss That Are Correlated With Behavioral Deficits JO: ASN Neuro http://www.kidney.de/pget.php?&tw=1&pmid=29932344 #FOAvip An estimated 5.3 million Americans are living with a disability from a traumatic brain injury (TBI). There is emerging evidence of the detrimental effects from repeated mild TBIs (rmTBIs). rmTBI manifests its own unique set of behavioral and neuropathological changes. A subset of individuals exposed to rmTBI develop permanent behavioral and pathological consequences, defined postmortem as chronic traumatic encephalopathy. We have combined components of two classic rodent models of TBI, the controlled cortical impact model and the weight drop model, to develop a repeated mild closed head injury (rmCHI) that produces long-term deficits in several behaviors that correlate with neuropathological changes. Mice receiving rmCHI performed differently from 1-hit or sham controls on the elevated plus maze; these deficits persist up to 6 months postinjury (MPI). rmCHI mice performed worse than 1-hit and control sham mice at 2 MPI and 6 MPI on the Morris water maze. Mice receiving rmCHI exhibited significant atrophy of the corpus callosum at both 2 MPI and 6 MPI, as assessed by stereological volume analysis. Stereological analysis also revealed significant loss of cortical neurons in comparison with 1-hit and controls. Moreover, both of these pathological changes correlated with behavioral impairments. In human tau transgenic mice, rmCHI induced increases in hyperphosphorylated paired helical filament 1 tau in the hippocampus. This suggests that strategies to restore myelination or reduce neuronal loss may ameliorate the behavioral deficits observed following rmCHI and that rmCHI may model chronic traumatic encephalopathy in human tau mice. Twit Text FOAVip Repeated Mild Closed Head Injuries Induce Long-Term White Matter Pathology and Neuronal Loss That Are Correlated With Behavioral Deficits ????ASN Neuro http://www.kidney.de/pget.php?&tw=1&pmid=29932344 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29932344 #FOAvip English Wikipedia <ref>{{Cite pmid|29932344 }}</ref> Repeated Mild Closed Head Injuries Induce Long-Term White Matter Pathology and Neuronal Loss That Are Correlated With Behavioral Deficits #MMPMID29932344 Gold EM ; Vasilevko V ; Hasselmann J ; Tiefenthaler C ; Hoa D ; Ranawaka K ; Cribbs DH ; Cummings BJ ASN Neuro 2018[Jan]; 10 (ä): 1759091418781921 PMID29932344 show ga An estimated 5.3 million Americans are living with a disability from a traumatic brain injury (TBI). There is emerging evidence of the detrimental effects from repeated mild TBIs (rmTBIs). rmTBI manifests its own unique set of behavioral and neuropathological changes. A subset of individuals exposed to rmTBI develop permanent behavioral and pathological consequences, defined postmortem as chronic traumatic encephalopathy. We have combined components of two classic rodent models of TBI, the controlled cortical impact model and the weight drop model, to develop a repeated mild closed head injury (rmCHI) that produces long-term deficits in several behaviors that correlate with neuropathological changes. Mice receiving rmCHI performed differently from 1-hit or sham controls on the elevated plus maze; these deficits persist up to 6 months postinjury (MPI). rmCHI mice performed worse than 1-hit and control sham mice at 2 MPI and 6 MPI on the Morris water maze. Mice receiving rmCHI exhibited significant atrophy of the corpus callosum at both 2 MPI and 6 MPI, as assessed by stereological volume analysis. Stereological analysis also revealed significant loss of cortical neurons in comparison with 1-hit and controls. Moreover, both of these pathological changes correlated with behavioral impairments. In human tau transgenic mice, rmCHI induced increases in hyperphosphorylated paired helical filament 1 tau in the hippocampus. This suggests that strategies to restore myelination or reduce neuronal loss may ameliorate the behavioral deficits observed following rmCHI and that rmCHI may model chronic traumatic encephalopathy in human tau mice. |Animals [MESH] |Calcium-Binding Proteins/metabolism [MESH] |Disease Models, Animal [MESH] |Head Injuries, Closed/*complications/*pathology [MESH] |Hindlimb Suspension [MESH] |Longitudinal Studies [MESH] |Male [MESH] |Maze Learning [MESH] |Mental Disorders/*etiology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Microfilament Proteins/metabolism [MESH] |Nerve Tissue Proteins/metabolism [MESH] |Neurons/*pathology [MESH] |Swimming [MESH] |White Matter/*pathology [MESH]Repeated Mild Closed Head Injuries Induce Long-Term White Matter Patho(epmc).pdf DeepDyve Pubget Overpricing