Neuroscience
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Fatigue in people with Multiple Sclerosis (PwMS) is a poorly understood, complex, and disabling symptom. We hypothesized that the perception of fatigue in PwMS results from increased information processing in cortical areas responsible for the perception of bodily states and decreased information processing in the cortico-basal ganglia network involved in the perception of motor performance. We investigated whether PwMS who perceive excessive fatigue would have increased resting-state functional connectivity (rsFC) between interoceptive brain areas (amygdala, anterior cingulate cortex [ACC], and insula) and decreased rsFC between cortico-basal ganglia premotor network compared to PwMS not reporting fatigue. ⋯ The Modified Fatigue Impact Scale scores were correlated with the increased rsFC between interoceptive brain areas (amygdala and insula) and decreased rsFC between cortico-basal ganglia (P < 0.01). MS-related perceived fatigue has a central cause, and it may be due to increased interoceptive brain activity (perception of bodily states). Interventions are needed to decrease fatigue and reorganize the brain circuitry.
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Review Meta Analysis
The tryptophan catabolite or kynurenine pathway in Long COVID disease: A systematic review and meta-analysis.
Recent studies confirm the involvement of activated immune-inflammatory responses and increased oxidative and nitrosative stress in Long COVID (LC) disease. However, the influence of these pathways on the metabolism of tryptophan (TRP) through the TRP catabolite (TRYCAT) pathway and their mediating effects on LC pathophysiology, has not been fully explored. ⋯ The current findings suggest that an activated TRYCAT pathway, characterized by decreased TRP levels and maybe elevated KYN levels, plays a significant role in the pathophysiology of LC.
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A common anatomical core has been described for psychiatric disorders, consisting of the dorsal anterior cingulate cortex (dACC) and anterior insula, processing uncertainty. A common neurophysiological core has been described for other brain related disorders, called thalamocortical dysrhythmia (TCD), consisting of persistent cross-frequency coupling between low and high frequencies. And a common genetic core has been described for yet another set of hypodopaminergic pathologies called reward deficiency syndromes (RDS). ⋯ TCD and RDS share a common anatomical and neurophysiological core, consisting of beta activity in the dACC and theta activity in dACC extending into precuneus and dorsolateral prefrontal cortex. TCD and RDS differ in pgACC/vmPFC activity and demonstrate an opposite balance between pgACC/vmPFC and dACC. Based on the Bayesian brain model TCD and RDS can be defined as uncertainty disorders in which the pgACC/vmPFC and dACC have an opposite balance, possibly explained by an inverted-U curve profile of both pgACC/vmPFC and dACC.
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Review Meta Analysis
Perinatal anoxia associated with sensorimotor restriction causes muscle atrophy and microglial activation: Meta-analysis of preclinical studies with implications for cerebral palsy.
Several experimental cerebral palsy models have been created to investigate cellular and molecular mechanisms involved in this condition and develop new therapeutic strategies. The model that has come closest to a motor phenotype similar to cerebral palsy is the one that combines perinatal anoxia with hindlimb sensorimotor restriction, as it induces visible changes at the peripheral and central levels. This systematic review with meta-analysis presents the impact of the cerebral palsy model that associates perinatal anoxia with hindlimb sensorimotor restriction on the nervous, muscular and skeletal systems. ⋯ The results of the meta-analysis reported a significant reduction in the media area of the soleus muscle fibers, increased number of glia cells and glia/neuron index in the somatosensory cortex, increased microglial activation in the hippocampus, and no changes in the corpus callosum thickness or neuron cells. The combination of perinatal anoxia and sensorimotor restriction entails muscle deficits and excessive activation of glial cells in brain areas. These results contribute to a methodological refinement of cerebral palsy models and favor new studies proposed for methodological elucidation in animal experimentation.
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Numerous studies linking environmental pollutants to oxidative stress, inflammation, and neurotoxicity have assigned pollutants to several neurodegenerative disorders, including Alzheimer's disease (AD). Heavy metals, pesticides, air pollutants, and endocrine disruptor chemicals have been shown to play important roles in AD development, with some traditional functions in amyloid-β formation, tau kinase action, and neuronal degeneration. However, pharmacological management and supplementation have resulted in limited improvement. ⋯ Furthermore, they contribute to positive changes in the composition of the human gut microbiota and thus encourage interactions in the Gut-Brain Axis, reducing inflammation caused by pollutants. This review emphasizes a multi-professional approach with reference to nutritional activities that would lower the neurotoxic load in populations with a high level of exposure to pollutants. Future studies focusing on diet and environment association plans may help identify preventive measures aimed at enhancing current disease deceleration.