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Enrique Luengo Izaskun Buendia Cristina Fernndez‐Mendívil Paula Trigo‐Alonso Pilar Negredo Patrycja Michalska Borja Hernndez‐García Cristina Snchez‐Ramos Juan A. Bernal Tsuneya Ikezu Rafael Len Manuela G. Lpez 《Journal of pineal research》2019,67(1)
Alterations in autophagy are increasingly being recognized in the pathogenesis of proteinopathies like Alzheimer's disease (AD). This study was conducted to evaluate whether melatonin treatment could provide beneficial effects in an Alzheimer model related to tauopathy by improving the autophagic flux and, thereby, prevent cognitive decline. The injection of AAV‐hTauP301L viral vectors and treatment/injection with okadaic acid were used to achieve mouse and human ex vivo, and in vivo tau‐related models. Melatonin (10 μmol/L) impeded oxidative stress, tau hyperphosphorylation, and cell death by restoring autophagy flux in the ex vivo models. In the in vivo studies, intracerebroventricular injection of AAV‐hTauP301L increased oxidative stress, neuroinflammation, and tau hyperphosphorylation in the hippocampus 7 days after the injection, without inducing cognitive impairment; however, when animals were maintained for 28 days, cognitive decline was apparent. Interestingly, late melatonin treatment (10 mg/kg), starting once the alterations mentioned above were established (from day 7 to day 28), reduced oxidative stress, neuroinflammation, tau hyperphosphorylation, and caspase‐3 activation; these observations correlated with restoration of the autophagy flux and memory improvement. This study highlights the importance of autophagic dysregulation in tauopathy and how administration of pharmacological doses of melatonin, once tauopathy is initiated, can restore the autophagy flux, reduce proteinopathy, and prevent cognitive decline. We therefore propose exogenous melatonin supplementation or the development of melatonin derivatives to improve autophagy flux for the treatment of proteinopathies like AD. 相似文献
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Elizabeth M. Broad Laura J. Newsome Dustin A. Dew 《The journal of spinal cord medicine》2020,43(3):388-397
Objective: Report measured resting energy expenditure (REE) in wheelchair rugby athletes and evaluate agreement between REE and the prediction models of Chun, Cunningham, Harris-Benedict, Mifflin, Nightingale and Gorgey, and Owen.Design: Cohort-based validation study.Setting. Paralympic team training camp.Participants: Fourteen internationally competitive athletes who play wheelchair rugby, 13 of whom had cervical spinal cord injuries (SCI).Outcome Measures: A portable metabolic analyzer was used to measure REE following an overnight fast and dual-energy X-ray absorptiometry (DXA) was used to assess lean body mass for the prediction equations.Results: REE in the current sample was 1735?±?257?kcal?×?day?1 ranging from 1324 to 2068?kcal?×?day?1. Bland–Altman analyses revealed negative mean bias but similar limits of agreement between measured REE and scores predicted by Chun, Cunningham, Mifflin, Nightingale and Gorgey, and Owen models in elite athletes who play wheelchair rugby.Conclusion: Prediction models regressed on persons with and without SCI under-predicted REE of competitive wheelchair rugby athletes. This outcome may be explained by the higher REE/fat-free mass (FFM) ratio of current athletes compared to less active samples. Findings from the current study will help practitioners to determine nutrient intake needs on training days of varied intensity. 相似文献
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