Neuroscience
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Randomized Controlled Trial
Fronto-Parietal Brain Areas Contribute to the Online Control of Posture during a Continuous Balance Task.
Neuroimaging studies have provided evidence for the involvement of frontal and parietal cortices in postural control. However, the specific role of these brain areas for postural control remains to be known. Here, we investigated the effects of disruptive transcranial magnetic stimulation (TMS) over supplementary motor areas (SMA) during challenging continuous balance task in healthy young adults. ⋯ Importantly, cTBS over SMA compared to sham stimulation altered EEG power within the identified fronto-parietal regions. These findings suggest that the changes in activation within distant fronto-parietal brain areas following cTBS over SMA contributed to the altered postural behavior. Our study confirms a critical role of AC, CG, and both PPC regions in calibrating online postural responses during a challenging continuous balance task.
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Is sentence structure processed by the same neural and cognitive resources that are recruited for processing word meanings, or do structure and meaning rely on distinct resources? Linguistic theorizing and much behavioral evidence suggest tight integration between lexico-semantic and syntactic representations and processing. However, most current proposals of the neural architecture of language continue to postulate a distinction between the two. One of the earlier and most cited pieces of neuroimaging evidence in favor of this dissociation comes from a paper by Dapretto and Bookheimer (1999). ⋯ Using a combination of whole-brain, group-level ROI, and participant-specific functional ROI approaches, we fail to replicate the original dissociation. In particular, whereas parts of LIFG respond reliably more strongly during lexico-semantic than syntactic processing, no part of LIFG (including in the region defined around the peak reported by Dapretto & Bookheimer) shows the opposite pattern. We speculate that the original result was a false positive, possibly driven by a small subset of participants or items that biased a fixed-effects analysis with low power.
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Coagulation factor XII (FXII) is synthesized in the liver and secreted into the circulation, where it initiates the contact activation system. Although typically thought to be restricted to the circulation, FXII protein has been found in the brain of Alzheimer's disease (AD) and multiple sclerosis patients. Moreover, activation of the contact system has been detected in the cerebrospinal fluid of these patients as well as in the brain of healthy and AD individuals. ⋯ We show that a recombinant version of this shorter FXII protein is activated by plasma kallikrein, reciprocally activates prekallikrein, and converts pro-hepatocyte growth factor (HGF) to active HGF in vitro. HGF-Met signaling plays a role in neuronal development and survival, and its dysregulation has been implicated in neurodevelopmental disorders and neurodegeneration. Taken together, our results show that a short isoform of FXII mRNA is expressed in the brain and raise the possibility that brain-derived FXII may be involved in HGF-Met signaling in neurons.
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Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E2 (PGE2), during seizures. ⋯ Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE2/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE2-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGE2 and PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.
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Alterations in early environmental conditions that interfere with the creation of a stable mother-pup bond have been suggested to be a risk factor for the development of stress-related psychopathologies later in life. The long-lasting effects of early experiences are mediated by changes in various cerebral circuits, such as the corticolimbic system, which processes aversive and rewarding stimuli. However, it is evident that the early environment is not sufficient per se to induce psychiatric disorders; interindividual (eg, sex-based) differences in the response to environmental challenges exist. ⋯ To this end, we assessed the behavioral phenotype of RCF and control (male and female) mice in the saccharine preference test and cocaine-induced conditioned place preference to evaluate the response to natural and pharmacological stimuli and in the elevated plus maze test and forced swimming test to measure their anxiety- and depression-like behavior. We also evaluated FST-induced c-Fos immunoreactivity in various brain regions that are engaged in the response to acute stress exposure (FST). Notably, RCF has opposing effects on the adult response to these tests between sexes, directing male mice toward an "anhedonia-like" phenotype and increasing the sensitivity for rewarding stimuli in female mice.