Neuroscience
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How is motor learning affected by aging? Although several experimental paradigms have been used to address this question, there has been limited focus on the early phase of motor learning, which involves motor exploration and the need to coordinate multiple degrees of freedom in the body. Here, we examined motor learning in a body-machine interface where we measured both age-related differences in task performance as well as the coordination strategies underlying this performance. Participants (N = 65; age range 18-72 years) wore wireless inertial measurement units on the upper body, and learned to control a cursor on a screen, which was controlled by motions of the trunk. ⋯ However, we also found that these changes were associated with limited exploration in older adults. Moreover, when considering data across a majority of the lifespan (including children), longer movement times were associated with greater inefficiency of the coordination pattern, producing more task-irrelevant motion. These results suggest exploration behaviors during motor learning are affected with aging, and highlight the need for different practice strategies with aging.
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Neuroinflammation is considered to be a critical component in the pathological process after intracerebral hemorrhage (ICH). Microglia are the foremost and earliest inflammatory cells participating in the pathological process of ICH. AdipoRon is the agonist of AdipoR1 (Adiponectin receptor 1), which enhances P-AMPK (phosphorylated AMP-activated protein kinase) activation. ⋯ The in vitro experiment showed that AdipoRon not only directly inhibited neuronal ROS overproduction, but also indirectly decreased the neuronal death in a transwell co-culture system. In summary, AdipoRon protects against ICH induced injury through promoting M2a microglia polarization and reducing neuronal death. These effects of AdipoRon rely on the activation of AdipoR1-AMPK signaling pathway.
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A single session of aerobic exercise may offer one means to "prime" motor regions to be more receptive to the acquisition of a motor skill; however, the mechanisms whereby this priming may occur are not clear. One possible explanation may be related to the post-translational modification of plasticity-related receptors and their associated intracellular signaling molecules, given that these proteins are integral to the development of synaptic plasticity. In particular, phosphorylation governs the biophysical properties (e.g., Ca2+ conductance) and the migratory patterns (i.e., trafficking) of plasticity-related receptors by altering the relative density of specific receptor subunits at synapses. ⋯ We observed a robust (1.2-2.0× greater than sedentary) increase in tyrosine phosphorylation of AMPA (GluA1,2) and NMDA (GluN2A,B) receptor subunits, and a clear indication that exercise preferentially affects pPKA over pCaMKII. The changes were found, specifically, following moderate, but not maximal, acute aerobic exercise in both motor cortex and hippocampus. Given the requirement for these proteins during the early phases of plasticity induction, the possibility exists that exercise-induced priming may occur by altering the phosphorylation of plasticity-related proteins.
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Randomized Controlled Trial
Acute Exercise at Different Intensities Influences Corticomotor Excitability and Performance of a Ballistic Thumb Training Task.
The response to motor training is improved when preceded by a bout of aerobic exercise. However, the effect of exercise at different intensities on motor performance is not well understood. The aim of the current study was therefore to compare the neurophysiological and functional response to training with a ballistic abduction task following a single 30-min bout of low intensity continuous cycling exercise, high-intensity interval cycling exercise, or rest. ⋯ Finally, low-intensity exercise resulted in improved ballistic motor performance on both days. Our findings provide some evidence to suggest that low-intensity aerobic cycling is beneficial for performance during subsequent ballistic training. Furthermore, the effects of exercise intensity on motor training may depend on the type of task performed.
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Since the landmark discovery that point mutations in the α-synuclein gene (SNCA) cause familial Parkinson's disease (PD) more than 2 decades ago, extensive research has been conducted to unravel the molecular and cellular mechanisms by which α-synuclein drives PD pathogenesis resulting in selective neurodegeneration of vulnerable neuronal populations. Current interest focuses on the identification of relevant toxic α-synuclein conformers and their interaction with basic cellular functions. ⋯ In this short review, we focus on cell-specific responses to α-synuclein with a focus on the toxic conformers of α-synuclein. We will not discuss more general cellular death pathways, which have been comprehensively covered by a number of elegant recent reviews.