Low-Field Magnetic Stimulation Restores Cognitive and Motor Functions in the Mouse Model of Repeated Traumatic Brain Injury: Role of Cellular Prion Protein

2019 ◽  
Vol 36 (22) ◽  
pp. 3103-3114 ◽  
Author(s):  
Sathiya Sekar ◽  
Yanbo Zhang ◽  
Hajar Miranzadeh Mahabadi ◽  
Amirhassan Parvizi ◽  
Changiz Taghibiglou
2017 ◽  
Vol 63 ◽  
pp. 197-209 ◽  
Author(s):  
Vibol Chhor ◽  
Raffaella Moretti ◽  
Tifenn Le Charpentier ◽  
Stephanie Sigaut ◽  
Sophie Lebon ◽  
...  

2021 ◽  
Vol 22 (16) ◽  
pp. 9005
Author(s):  
Sathiya Sekar ◽  
Raja Solomon Viswas ◽  
Hajar Miranzadeh Mahabadi ◽  
Elahe Alizadeh ◽  
Humphrey Fonge ◽  
...  

Brain injury/concussion is a growing epidemic throughout the world. Although evidence supports association between traumatic brain injury (TBI) and disturbance in brain glucose metabolism, the underlying molecular mechanisms are not well established. Previously, we reported the release of cellular prion protein (PrPc) from the brain to circulation following TBI. The PrPc level was also found to be decreased in insulin-resistant rat brains. In the present study, we investigated the molecular link between PrPc and brain insulin resistance in a single and repeated mild TBI-induced mouse model. Mild TBI was induced in mice by dropping a weight (~95 g at 1 m high) on the right side of the head. The procedure was performed once and thrice (once daily) for single (SI) and repeated induction (RI), respectively. Micro PET/CT imaging revealed that RI mice showed significant reduction in cortical, hippocampal and cerebellum glucose uptake compared to SI and control. Mice that received RI also showed significant motor and cognitive deficits. In co-immunoprecipitation, the interaction between PrPc, flotillin and Cbl-associated protein (CAP) observed in the control mice brains was disrupted by RI. Lipid raft isolation showed decreased levels of PrPc, flotillin and CAP in the RI mice brains. Based on observation, it is clear that PrPc has an interaction with CAP and the dislodgment of PrPc from cell membranes may lead to brain insulin resistance in a mild TBI mouse model. The present study generated a new insight into the pathogenesis of brain injury, which may result in the development of novel therapy.


Author(s):  
Richard Rubenstein ◽  
Binggong Chang ◽  
Natalia Grinkina ◽  
Eleanor Drummond ◽  
Peter Davies ◽  
...  

Author(s):  
Sandrine Bourgeois-Tardif ◽  
Louis De Beaumont ◽  
José Carlos Rivera ◽  
Sylvain Chemtob ◽  
Alexander G Weil

BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.


2021 ◽  
Vol 556 ◽  
pp. 149-155
Author(s):  
Lu Huang ◽  
Shulei He ◽  
Qing Cai ◽  
Fei Li ◽  
Siwei Wang ◽  
...  

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