Neuroscience
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For a long time, traditional medicine has acknowledged the gut's impact on general health. Contemporary science substantiates this association through investigations of the gut microbiota, the extensive community of microorganisms inhabiting our gastrointestinal system. These microscopic residents considerably improve digestive processes, nutritional absorption, immunological function, and pathogen defense. ⋯ We also conducted a thorough examination of the existing understanding in the area of how microbiota affects social behaviors, including emotions, stress responses, and cognitive functions. We also explored the potential of interventions that focus on the connection between the gut and the brain, such as using probiotics to treat diseases of the CNS. This research opens up new possibilities for addressing mental health and neurological conditions in an innovative manner.
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Sleep deprivation is a prevalent issue in contemporary society, with significant ramifications for both physical and mental well-being. Emerging scientific evidence illuminates its intricate interplay with the gut-brain axis, a vital determinant of neurological function. Disruptions in sleep patterns disturb the delicate equilibrium of the gut microbiota, resulting in dysbiosis characterized by alterations in microbial composition and function. ⋯ Moreover, the advent of personalized interventions guided by advanced omics technologies holds considerable potential for tailoring treatments to individualized needs and optimizing therapeutic outcomes. Interdisciplinary collaboration and concerted research efforts are imperative for elucidating the underlying mechanisms linking sleep, gut microbiota, and neurological function. Longitudinal studies, translational research endeavours, and advancements in technology are pivotal for unravelling the complex interplay between these intricate systems.
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Parkinson's disease is one of the most prevalent neurodegenerative motor disorders worldwide with postural instability, bradykinesia, resting tremor and rigidity being the most common symptoms of the disease. Despite the fact that the molecular mechanisms of Parkinson's disease pathogenesis have already been well described, there is still no coherent picture of the etiopathogenesis of this disease. According to modern concepts, neurodegeneration is induced mainly by oxidative stress, neuroinflammation, dysregulation of cerebral proteostasis, apoptotic dysregulation, and impaired autophagy. ⋯ The review also discusses the role of calpains in the development of Parkinson's disease. It is known that α-synuclein is a substrate of calcium-dependent proteases of the calpain family. Truncated forms of α-synuclein are not only involved in the process of formation of the aggregates, but also increase their toxicity.
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This article discusses the peculiarities of microglia behaviour and their interaction with other cells of the central nervous system (CNS) during neural tissue injury with a focus on spinal cord injury (SCI). Taking into account the plasticity of microglia, the influence of the microenvironment should be taken into account to establish the mechanisms determining the polarization pathways of these cells. ⋯ This review compiles information on changes in microglia activation, migration and phagocytosis, as well as their reciprocal effects on other CNS cells, such as neurons, astrocytes and oligodendrocytes, in the background of SCI. The information contained in this article may be of interest not only to scientists studying traumatic injuries of the central nervous system, but also to specialists in the field of studying and treating neurodegenerative diseases, since the mechanisms occurring in the injured spinal cord may also be characteristic of pathological events in degenerative processes.
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Review
Multifaceted roles of DLG3/SAP102 in neurophysiology, neurological disorders and tumorigenesis.
DLG3, also known as Synapse-associated protein 102 (SAP102), is essential for the organization and plasticity of excitatory synapses within the central nervous system (CNS). It plays a critical role in clustering and moving key components necessary for learning and memory processes. Mutations in the DLG3 gene, which result in truncated SAP102 proteins, have been associated with a range of neurological disorders, including X-linked intellectual disability (XLID), autism spectrum disorders (ASD), and schizophrenia, all of which can disrupt synaptic structure and cognitive functions. ⋯ Moreover, SAP102 has been demonstrated to regulate tumor-induced bone pain through activating NMDA receptors. These findings highlight SAP102 as a promising therapeutic target for both neurological disorders and cancer. Therefore, further investigation into the regulatory roles of SAP102 in neural development and disease may lead to novel therapeutic approaches for treating synaptic disorders and managing cancer progression.