Neuroscience
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The Stroop test is a widely used neuropsychological test measuring attention and conflict resolution, which shows sensitivity across a range of diseases, including Alzheimer's, Parkinson's and Huntington's diseases. A rodent analogue of the Stroop test, the Response-Conflict task (rRCT), allows for systematic investigation of the neural systems underpinning performance in this test. Little is known about the involvement of the basal ganglia in this neural process. ⋯ Involvement of the basal ganglia in this neural process has not previously been reported. These data demonstrate that the cognitive process of conflict resolution requires not only prefrontal cortical regions, but also recruits the dysgranular retrosplenial cortex and the medial region of the neostriatum. These data have implications for understanding the neuroanatomical changes that underpin impaired Stroop performance in people with neurological disorders.
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease related to the progressive death of motor neurons. Understanding the pathogenesis of ALS continues to provide considerable challenges. Bulbar-onset ALS involves faster functional loss and shorter survival time than spinal cord-onset ALS. ⋯ This miRNA was found to directly target ERBB4 and regulate the AKT/GSK3β pathway. Collectively, the above miRNAs and their targets are related to the development of bulbar-onset ALS. Our research indicates that miR-23a-3p might have an effect on motor neuron loss observed in bulbar-onset ALS and may be a novel target for the therapy of ALS in the future.
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The frontoparietal network (FPN) and cingulo-opercular network (CON) may exert top-down regulation corresponding to the central executive system (CES) in working memory (WM); however, contributions and regulatory mechanisms remain unclear. We examined network interaction mechanisms underpinning the CES by depicting CON- and FPN-mediated whole-brain information flow in WM. We used datasets from participants performing verbal and spatial working memory tasks, divided into encoding, maintenance, and probe stages. ⋯ Task-level output was slightly stronger for the CON. CON → FPN, CON → DMN, visual areas → CON, and visual areas → FPN showed consistent effects. The CON and FPN might together underlie the CES's neural basis and achieve top-down regulation through information interaction with other large-scale functional networks, and the CON may be a higher-level regulatory core in WM.
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Memories already consolidated when reactivated return to a labile state and can be modified, this process is known as reconsolidation. It is known the Wnt signaling pathways can modulate hippocampal synaptic plasticity as well as learning and memory. Yet, Wnt signaling pathways interact with NMDA (N-methyl-D-aspartate) receptors. ⋯ Moreover, the impairment induced by DKK1 was blocked by the administration of the agonist of the NMDA receptors glycine site, D-Serine, immediately and 2 h after reactivation session. We found that hippocampal canonical Wnt/β-catenin is necessary to the reconsolidation of CFC memory at least two hours after reactivation, while non-canonical Wnt/Ca2+ signaling pathway is not involved in this process and, that there is a link between Wnt/β-catenin signaling pathway and NMDA receptors. In view of this, this study provides new evidence regarding the neural mechanisms underlying contextual fear memory reconsolidation and contributes to provide a new possible target for the treatment of fear related disorders.
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Functional magnetic resonance imaging (fMRI) is a convolution of latent neural activity and the hemodynamic response function (HRF). According to prior studies, the neurodegenerative process in idiopathic Parkinson's Disease (PD) interacts significantly with neuromuscular abnormalities. Although these underlying neuromuscular changes might influence the temporal characteristics of HRF and fMRI signals, relatively few studies have explored this possibility. ⋯ The results suggested that neglecting HRF variability may cultivate false-positive and false-negative FC group differences. Furthermore, HRF was related to dopamine receptor type 2 (DRD2) gene expression (P < 0.001, t = -7.06, false discover rate-corrected). Taken together, these findings reveal HRF variation and its possible underlying molecular mechanism in PD, and suggest that deconvolution could reduce the impact of HRF variation on FC group differences.