Neuroscience
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Comparative Study
Age-induced differences in brain neural activation elicited by visual emotional stimuli: A High-Density EEG study.
Identifying the brain sources of neural activation during processing of emotional information remains a very challenging task. In this work, we investigated the response to different emotional stimuli and the effect of age on the neuronal activation. Two negative emotion conditions, i.e., 'anger' and 'fear' faces were presented to 22 adult female participants (11 young and 11 elderly) while acquiring high-density electroencephalogram (EEG) data of 256 channels. ⋯ Furthermore, age-induced differences are shown in the topographic maps and the neural activation for both emotional stimuli. Overall, aging appeared to affect the limbic area and its implication to emotional processing. These findings can serve as a step toward the understanding of the way the brain functions and evolves with age which is a significant element in the design of assistive environments.
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Previous research has suggested that balance impairments may be linked to anxiety in PD, yet there is little empirical evidence to support this link in PD. This study aimed to evaluate the influence of anxiety on balance, and also examine whether dopaminergic treatment modulates the influence of anxiety on balance. Forty-two participants (10 high anxious PD [HA-PD]; 11 low anxious PD [LA-PD], 21 controls [HC]) performed 10 quiet standing trials on a force platform in two virtual environments: LOW threat; on a plank located on the ground; HIGH threat; on an elevated plank. ⋯ Although dopaminergic medication significantly reduced self-reported anxiety, it had limited effects on balance. In conclusion, this study provides strong evidence that anxiety does influence balance control in PD, especially those who are highly anxious. Dopamine appears to modulate anxiety, but further research is needed to evaluate whether dopaminergic treatment is optimal for anxiety induced balance deficits.
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Sandhoff disease (SD) is a lysosomal storage disorder characterized by the absence of hydrolytic enzyme β-N-acetylhexosaminidase (Hex), which results in storage of GM2 ganglioside in neurons and unremitting neurodegeneration. Neuron loss initially affects fine motor skills, but rapidly progresses to loss of all body faculties, a vegetative state, and death by five years of age in humans. A well-established feline model of SD allows characterization of the disease in a large animal model and provides a means to test the safety and efficacy of therapeutic interventions before initiating clinical trials. ⋯ SD cats were treated with intracranial delivery of adeno-associated viral (AAV) vectors expressing feline Hex, with a study endpoint 16weeks post treatment. AAV-mediated gene delivery repressed the expansion and activation of microglia and normalized MHC-II and MIP-1α levels. These data reiterate the profound inflammatory response in SD and show that neuroinflammation is abrogated after AAV-mediated restoration of enzymatic activity.
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Neuronal gap junctions are ubiquitous in the brain, but their precise positions in actual neuronal circuits have been uncertain, and their functional roles remain unclear. In this study, I visualized connexin36-immunoreactive gap junctions and examined the structural features of the interconnected dendrites arising from parvalbumin (PV)-positive interneurons in layer 4 of the feline visual cortex. I observed evidence for net-like dense linkages of dendrites among virtually all PV neurons (56/58 cells, 96.6%) in the tissue. ⋯ In contrast, gap junctions formed between nearby cells were close to both somata. Thalamocortical afferents established synapses densely on somata of layer 4 PV neurons, indicating the possible involvement of proximal gap junctions in visual stimulus-driven feedforward regulation. These findings provide a new structural basis for cortical investigations.
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Equivocal evidence indicates that high-intensity muscle contractions can affect the corticospinal responses in muscles not directly involved in the task. In the present study, the responsiveness of corticomotor pathway innervating non-dominant biceps brachii was measured in eleven healthy participants before and after: (i) two 100-s isometric unilateral knee extension maximal voluntary contractions (MVCs) on dominant leg (FATIGUE) and (ii) rest (CONTROL). Transcranial magnetic stimulation, transmastoid electrical and brachial plexus electrical stimulation were used to evoke motor evoked potential (MEP), cervicomedullary motor evoked potential (CMEP) and compound muscle action potential (Mmax) in biceps brachii muscle. ⋯ Yet, the elbow flexor MVC force did not exhibit any difference between FATIGUE and CONTROL conditions. These results suggest that the upper limb muscles' corticomotor pathway responsiveness recorded during voluntary contractions were modulated by lower limbs fatiguing contractions and this modulation depends on the force produced during testing, i.e. level of central motor drive. However, these changes have little effect on upper limb muscle maximal performance.