Neuroscience
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Review
Virtual reality modulating dynamics of neuroplasticity: Innovations in neuro-motor rehabilitation.
Virtual reality (VR) technology has emerged as a ground-breaking tool in neuroscience, revolutionizing our understanding of neuroplasticity and its implications for neurological rehabilitation. By immersing individuals in simulated environments, VR induces profound neurobiological transformations, affecting neuronal connectivity, sensory feedback mechanisms, motor learning processes, and cognitive functions. These changes highlight the dynamic interplay between molecular events, synaptic adaptations, and neural reorganization, emphasizing the potential of VR as a therapeutic intervention in various neurological disorders. ⋯ Integrating molecular neuroscience with VR technology allows for a deeper understanding of the molecular mechanisms underlying neuroplasticity, opening doors to personalized interventions and precise treatment strategies for individuals with neurological impairments. Moreover, the review emphasizes the ethical considerations and challenges that come with implementing VR-based interventions in clinical practice, stressing the importance of data privacy, informed consent, and collaborative interdisciplinary efforts. By leveraging advanced molecular imaging techniques, VR-based research methodologies, and computational modelling, the review envisions a future where VR technology plays a central role in revolutionizing neuroscience research and clinical neurorehabilitation, ultimately providing tailored and impactful solutions for individuals facing neurological challenges.
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Apelin, an endogenous ligand of G protein-coupled receptor APJ, is widely distributed in the central nervous system (CNS). It can be divided into such subtypes as Apelin-13, Apelin-17, and Apelin-36 as they have different amino acid structures. ⋯ As an adipokine, Apelin has been found to play a crucial role in cardiovascular disease development. In this paper, we reviewed the effects and mechanisms of Apelin in treating CNS diseases, such as neurotrauma, stroke, spinal cord injury, primary tumors, neurodegenerative diseases, psychiatric diseases, epilepsy, and pain.
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It is becoming increasingly recognized that, in addition to psychological stress, unbalanced maternal nutritional habits can threaten fetal brain development. Maternal obesity is one of the most pressing public health problems facing the world today, as about 40% of pregnant women are obese or gain excessive weight worldwide. ⋯ We argue that maternal Omega-3 supplementation, among the many dietary strategies available, is especially promising as it buffers oxidative stress and inflammation, both recognized as candidate mechanisms underlying the negative long-term effects of maternal obesity on the offspring. Notwithstanding the current knowledge, both preclinical studies and clinical trials are needed to refine current strategies addressing dietary content and length of administration according to individual characteristics and needs.
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The aim of this study was to assess the potential causal relationship between lifestyle factors and intracranial aneurysms (IAs) using a two-sample Mendelian randomization (MR) approach. The study used a pooled dataset from a genome-wide association study that covered information on 24 lifestyle factors, intracranial aneurysm cases, subarachnoid hemorrhage, and unruptured aneurysms. Five MR methods were applied for analysis by selecting single nucleotide polymorphisms as instrumental variables, with the inverse variance weighting method as the main method. ⋯ Sensitivity analyses and inverse MR verified the robustness of these results. After adjusting for exposure factors, multivariate MR confirmed daily smoking and smoking initiation as risk factors for intracranial aneurysms, unruptured aneurysms, and subarachnoid hemorrhage, whereas red wine intake was a genetically protective factor against intracranial aneurysms and subarachnoid hemorrhage. This MR analysis revealed a genetic causal link between specific lifestyle factors and intracranial aneurysms, emphasizing the need for further studies to confirm these findings and explore their mechanisms.
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Alzheimer's disease (AD) is a growing health problem worldwide, particularly in the developed world due to an ageing population. Glutamate excitotoxicity plays a major role in the pathophysiology of AD, and glutamate re-uptake is controlled by excitatory amino acid transporters (EAATs). The EAAT2 isoform is the predominant transporter involved in glutamate reuptake, therefore EAAT1 has not been the focus of AD research. ⋯ Labeling of EAAT1 appeared astrocytic in nature, showing close association with astrocytic processes in AD cases. We also report that a higher EAAT1 density was positively correlated with the age of AD cases, but this relationship was not observed in control cases. Overall, our results indicate an upregulation of EAAT1 across several hippocampal subregions and layers in AD cases, indicating a potential physiological role for this transporter that needs further investigation.