Neuroscience
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In this study, we address the question: Can the central nervous system stabilize vertical posture in the abundant space of neural commands? We assume that the control of vertical posture is associated with setting spatial referent coordinates (RC) for the involved muscle groups, which translates into two basic commands, reciprocal and co-activation. We explored whether the two commands co-varied across trials to stabilize the initial postural state. Young, healthy participants stood quietly against an external horizontal load and were exposed to smooth unloading episodes. ⋯ Analysis of deviations in the {RC; k} space keeping the posture unchanged (motor equivalent) between two states separated by a voluntary quick body sway showed significantly larger motor equivalent deviations compared to non-motor equivalent ones. This is the first study demonstrating posture-stabilizing synergies in the space of neural control variables using various computational methods. It promises direct applications to studies of postural disorders and rehabilitation.
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Accumulating evidence indicates that repetitive transcranial magnetic stimulation (rTMS) ameliorates motor symptoms in patients with Parkinson's disease (PD); however, patients' responses to rTMS are different. Here, we aimed to explore neural activity changes in patients with PD exhibiting different responses to high-frequency rTMS treatments using functional magnetic resonance imaging (fMRI). We treated 24 patients with PD using 10-session rTMS (10 Hz) over the supplementary motor area (SMA) for 10 days. ⋯ We identified increased fALFF values in the left Crus II of the cerebellar hemisphere and bilateral thalamus as responsive signs to rTMS. Furthermore, the motor response to rTMS over the SMA, measured by the reduction in UPDRS-III and bradykinesia scores, was positively associated with increased fALFF values in the left Crus2 of cerebellar hemisphere, left lobule VIIB of cerebellar hemisphere, right lobule VI of the cerebellar hemisphere, and the right postcentral gyrus. These findings provide evidence for the involvement of cerebellar activity in the motor response to rTMS treatment.
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Dopamine facilitates approach to reward via its actions on dopamine receptors in the nucleus accumbens. For example, blocking either D1 or D2 dopamine receptors in the accumbens reduces the proportion of reward-predictive cues to which rats respond with cued approach. Recent evidence indicates that accumbens dopamine also promotes wakefulness and arousal, but the relationship between dopamine's roles in arousal and reward seeking remains unexplored. ⋯ Haloperidol reduced spontaneous locomotion but did not increase sleep postures, instead increasing immobility in non-sleep postures. We place these results in the context of the extensive literature on dopamine's contributions to behavior, and propose the arousal-motor hypothesis. This novel synthesis, which proposes that two main functions of dopamine are to promote arousal and facilitate motor behavior, accounts both for our findings and many previous behavioral observations that have led to disparate and conflicting conclusions.
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The pineal gland is a key player in surveillance and defense responses. In healthy conditions, nocturnal circulating melatonin (MEL) impairs the rolling and adhesion of leukocytes to the endothelial layer. Fungi, bacteria, and pro-inflammatory cytokines block nocturnal pineal MEL synthesis, facilitating leukocyte migration to injured areas. ⋯ There was an increase in cortical and no change in cerebellar MEL. These effects were mediated by changes in the expression of coding genes to synthetic and metabolizing melatonergic enzymes. Thus, the pineal gland plays a role as a first-line structure to respond to the death of cells inside the brain by turning NAS into the darkness hormone.
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Aging is a progressive loss of physiological function that increases risk of disease and death. Among the many factors that contribute to human aging, mitochondrial dysfunction has emerged as one of the most prominent features of the aging process. It has been linked to the development of various age-related pathologies, including Parkinson's disease (PD). ⋯ Even though research has shed light on several aspects of the disease pathology, the underlying mechanism of age-related factors responsible for individuals developing this disease is still unknown. This review article aims to discuss the role of mitochondria in the transition from normal brain aging to pathological brain aging, which leads to the progression of PD. We have discussed the emerging evidence on how age-related disruption of mitochondrial quality control mechanisms contributes to the development of PD-related pathophysiology.