Neuroscience
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Growing awareness of adverse impacts of artificial light on human health has led to recognize light pollution as a significant global environmental issue. Despite, a large number of studies in rodent and monkey models of Parkinson's disease have reported that near infrared light has neuroprotective effects on dopaminergic neurons, recent findings have shown that prolonged exposure of rodents and birds to fluorescent artificial light results in an increase of neuromelanin granules in substantia nigra and loss of dopaminergic neurons. ⋯ The present article discusses experimental evidence supporting a potentially deleterious impact of light on dopaminergic neurons and highlights the mechanisms whereby light might damage neuronal tissue. Moreover, it analyses epidemiological evidence that suggests light pollution to be an environmental risk factor for Parkinson's disease.
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Parkinson's disease (PD) is the second most common neurodegenerative disorder. Despite its high frequency the etiology is still unclear; several lines of evidence show that an inflammatory process is implicated in the pathogenesis of this disorder; where activation of brain microglia plays a central role in the damage of dopaminergic neurons of the substantia nigra. ⋯ This exposure may be enhanced by increased permeability of the intestinal ("leaky gut") and the blood brain barrier; enhancing the entrance of microbiota-produced substances into the central nervous system. In this manuscript, we explore the evidence from clinical and basic science implicating microglia activation by gut dysbiosis and how this phenomenon may impact in the symptomatology and progression of PD.
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Rotational uncertainty refers to the fact that the reaction time (RT) for identifying an upright stimulus is longer when the target stimulus is presented in a sequence of stimuli with different orientations (SU condition) than upright stimuli only (AU condition). Up until now, the rotational uncertainty effect has been only revealed by behavior measures, and its underlying neural mechanism remains unclear. In this study, using the hand mental rotation paradigm and electroencephalogram (EEG) recordings, we aimed to find the electrophysiological evidences of the rotational uncertainty from event-related potential (ERP) and event-related (de)synchronization (ERS/ERD) measurements. ⋯ Our results suggested that identifying the upright hand stimuli in SU condition induced more activation of motor networks, and the rotational uncertainty influenced multiple cognitive processes from the early visual processing to the late mental rotation and judging phases. The results implied that in SU condition, subjects might maintain readiness for the next possible mental rotation immediately after the previous response, with more attention to the coming visual stimuli. Even for the upright stimuli, they might still prepare for the mental rotation, and even mentally rotate the stimuli in a minor angle.
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Neurophysiological correlates of adaptation and interference during asymmetrical bimanual movements.
In this study, we investigated brain dynamics during interference between hands during bimanual movements. Participants performed a bimanual center-out reaching task in which a visuomotor rotation was applied to the right hand while the left hand did not receive visual feedback of its movements. This manipulation resulted in interference from the adapting right hand to the kinesthetically guided left hand. ⋯ This may be representative of error-based updating of internal models of movement. Additionally, coherence, a measure of neural functional connectivity, was elevated both within and between hemispheres in the beta frequencies during the initial presentation of the visuomotor rotation, and then decreased throughout adaptation. This suggests that beta oscillatory neural activity may be marker for transmission of conflicting motor information between hemispheres, which manifests in interference between the hands during asymmetrical bimanual movements.
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Survivals after prenatal hypoxia-ischemia (HI) usually suffer long-lasting cognitive defects. Reduced blood-oxygen supplies and the following reperfusion cause mitochondrial injury. Damaged mitochondria could be replaced by mitochondrial biogenesis program and peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) is the specific up-regulator. ⋯ Postnatal administration of pioglitazone further promoted PGC-1α and mitochondrial biogenesis, alleviated hippocampal injury, and improved performance in the behavioral tasks after intrauterine HI. Our investigation implicated activation of PGC-1α, and mitochondrial biogenesis is a neuroprotective mechanism against brain injury caused by systemic prenatal HI. Promotion of PGC-1α by pioglitazone might be a potential treatment for protecting against hippocampal injury and cognitive defects after intrauterine HI.