Neuroscience
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Fear of falling can have a profound influence on anticipatory postural control during dynamic balance tasks (e.g., rise-to-toes and leg-raise tasks), with fearful individuals typically exhibiting postural adjustments of smaller magnitudes prior to movement onset. However, very little is known about how fear of falling influences the generation of anticipatory postural adjustments (APAs) during gait initiation; a task in which producing smaller APAs may compromise stability. Sixteen young adults initiated gait as fast as possible following an auditory cue during two conditions: Baseline (ground level), and Threat (fear of falling induced via a platform raised 1.1 m). ⋯ We suggest that such failure to scale the APA to the magnitude of the motor output represents a fear-related 'overcompensation', whereby fearful participants sought to ensure that the APA was sufficient for ensuring that their centre of mass was positioned above the support leg prior to gait initiation. During conditions of threat, participants also exhibited greater postural sway prior to initiating gait (i.e., following the auditory cue) and took longer to generate the APA (i.e., impaired reaction). As greater reaction times during voluntary stepping is consistently associated with increased fall-risk, we suggest this as one mechanism through which fear of falling may reduce balance safety.
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Human visual function degrades with age. Previous studies of visual perception have shown that aged people have worse performance in the coding of orientation information. However, the neuronal mechanism still remains elusive. ⋯ Further investigation of neuronal correlation showed higher noise and signal correlations in aging monkeys than that in young monkeys. These correlation changes predicted a detrimental effect on the efficiency of population coding of orientation information. Taken together, our results suggest that the information coding efficiency of orientation information is impaired during aging and might account for the degradation of performance in human fine orientation discrimination task.
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Post-translational modification of Tau, a microtubule-associated protein in the neuronal cell, plays a major role in Alzheimer's disease. Tau is an axonal protein expressed in mature neurons that promote the self-assembly of tubulin into microtubules and its stabilization in neurons. Phosphorylation of Tau makes it prone to aggregation at the intra-neuronal region leading to impaired neurotransmission and dementia. ⋯ Here we highlight the role of GPCRs in Tau phosphorylation and Tau interaction in different cells of the nervous system. Hence, the role of GPCRs are attaining more attention in the therapeutic field of Alzheimer's disease. Specific agonists/antagonists and allosteric modulators could be the potential target for therapy against GPCR-mediated Tau phosphorylation in Alzheimer's disease.
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Cyclin-dependent kinase 5 (Cdk5) is a regulator of axon growth and radial neuronal migration in the developing mouse brain, and it plays critical roles in cortical structure formation and brain function. However, the function of Cdk5 in cortico-cortical and cortico-sensorimotor networks in the adult remains largely unknown. In this study, we investigated the function of Cdk5 in the rostral secondary motor cortex (M2) in the male mouse using CRISPR/Cas9 gene editing and somatic brain transgenesis, to produce M2-specific knockdown of Cdk5 in neurons in the male mouse. ⋯ Furthermore, whole-cell patch-clamp recordings in layer V green fluorescent protein (GFP)-tag pyramidal neurons revealed a decrease in the frequency and amplitude of miniature EPSCs and miniature IPSCs, as well as a reduction in the population synaptic responses (fEPSPs) in these mice. Specifically, retrograde labeling showed that Cdk5 knockdown in the M2 caused a reduction in long-range projections to the M2 from the thalamus/prefrontal cortex and claustrum. Collectively, our findings show a new regulatory role of Cdk5 in neural circuit maintenance, and that the changes in neural transmission and circuits in the mice with Cdk5 knockdown in the M2 likely contribute to the motor dysfunction in these animals.
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Randomized Controlled Trial
Early exercise after intracerebral hemorrhage inhibits inflammation and promotes neuroprotection in the sensorimotor cortex in rats.
The present study examined the effect of early exercise on brain damage and recovery of motor function following intracerebral hemorrhage (ICH) in rats. Subjects were randomly assigned to no training after ICH (ICH), no training after sham surgery (SHAM), early treadmill exercise after ICH (ICH + ET), and late treadmill exercise after ICH (ICH + LT) groups. The ICH + ET and ICH + LT groups were trained for seven consecutive days starting on day 2 and day 9 after surgery, respectively. ⋯ Expression of IL-1b mRNA was significantly lower in the ICH + ET group than that in the ICH group. Collectively, these results suggest that early treadmill exercise after ICH promotes recovery of sensorimotor function by preventing neuronal death and ensuing cortical atrophy and by preserving dendritic structure compared with late treadmill exercise and no exercise. Early exercise may prevent neurodegeneration and functional loss by inhibiting neuroinflammation.