Neuroscience
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Freezing of gait (FoG) is a brief, episodic absence or marked reduction of forward progression of the feet, despite the intention to walk, that is common in people with Parkinson's disease (PD). We hypothesized that not only motor, but higher level cognitive and attention areas may be impaired in freezers. In this study, we aimed to characterize differences in cortical and subcortical functional connectivity specific to FoG. ⋯ Associations between functional connectivity and objective measures of FoG were determined via predictive modeling using hold-out cross validation. We found that connectivity between the left globus pallidus (GP) and left somatosensory cortex and between two brain areas in the default and insular/vestibular networks exhibited significant differences specific to FoG and were also strong and significant predictors of FoG severity. Our findings suggest that the interplay among motor, default and vestibular areas of the left cortex are critical in the pathology of FoG.
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There is converging evidence that both aerobic exercise (AE) and transcranial direct current stimulation (tDCS) can acutely modulate executive functions (EF). In addition, recent studies have proposed the beneficial effects of applying tDCS during AE on physical performance. This study aimed to investigate whether tDCS applied during an AE session additionally or differently effects EF. ⋯ The nonsignificant effects of tDCS on EFs are in contrast to previous studies, as no replication of existing observations could be achieved. Thus, the protocol applied in this study does not provide any strong evidence that a combination of AE and tDCS has any effects on EFs, but indicates effects on physiological parameters and subjective exhaustion ratings. Further research should consider changes in AE and tDCS parameters (e.g., intensity or exercise mode) and sequence of applications (online vs. offline).
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After ischemic stroke, oxygen and nutrition depletion induce mitochondrial dysfunction, which aggravates brain injury. Bendavia, a mitochondria-targeted tetra-peptide, has anti-oxidative and anti-inflammatory activities. We previously reported that bendavia protected human brain microvascular endothelial cells against oxygen/glucose deprivation (OGD)-induced damage via preserving mitochondrial function. ⋯ In both models, bendavia inhibited neuronal cell death induced by OGD/R or H2O2. These findings indicated that bendavia attenuated brain ischemia/reperfusion damage and has direct neuroprotective effects against cell injury. Therefore, bendavia may be a novel therapeutic agent to improve ischemic stroke patient outcome.
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Strong stress related to adverse experiences during adolescence can cause mental disorders, as well as affecting brain structure and function. However, the underlying neurobiological mechanisms remain largely unknown. To investigate whether stress induced by adverse experience during adolescence affects oligodendrocyte (OL) remodeling, social defeat stress was applied to 6-week-old adolescent mice for 10 days, followed by behavioral tests and assessments of oligodendrogenesis. ⋯ Fewer bromodeoxyuridine-incorporated CC1-positive mature OLs were observed in these regions in socially defeated mice. To assess whether decreased oligodendrogenesis caused by social defeat stress is related to depressive-like symptoms under stress, clemastine, a drug that induces OL generation, was administered to socially defeated adolescent mice, resulting in the rescue of the behavioral abnormalities accompanied by increased oligodendrogenesis. These findings suggest that oligodendrogenesis in adverse environments during adolescence plays a role in psychiatric disorders, and clemastine may provide a potential therapeutic drug for adolescent mental disorders, targeting OLs.