Neuroscience
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Neurodegenerative disorders (NDDs) have been prevalent for more than a decade, and the number of individuals affected per year has increased exponentially. Among these NDDs, Alzheimer's disease, which causes extreme cognitive impairment, and Parkinson's disease, characterized by impairments in motor activity, are the most prevalent. While few treatments are available for clinical practice, they have minimal effects on reversing the neurodegeneration associated with these debilitating diseases. ⋯ The potential CRMs discussed in this review are quercetin, chrysin, astragalin, apigenin, curcumin, epigallocatechin-3-gallate, and NAD+ precursors. This review aims to provide an overview of these CRMs' effectiveness in preventing neurodegenerative disorders associated with aging. Moreover, we highlight the clinical relevance of these compounds by discussing in detail the results of clinical trials on them.
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Multiple sclerosis (MS) is a chronic, inflammatory demyelinating disorder of the central nervous system (CNS) targeting myelinated axons. Pathogenesis of MS entails an intricate genetic, environmental, and immunological interaction. Dysregulation of immune response i.e. autoreactive T & B-Cells and macrophage infiltration into the CNS leads to inflammation, demyelination, and neurodegeneration. ⋯ Therapeutic innovations have significantly transformed the management of MS, especially the use of disease-modifying therapies (DMTs) to reduce relapse rates and control disease progression. Advancements in research, neuroprotective strategies, and remyelination strategies hold promising results in reversing CNS damage. Various mice models are being adopted for testing new entities in MS research.
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Psychogenic erectile dysfunction (pED) is often accompanied by abnormal brain activities. This study aimed to develop an automaticclassifier to distinguish pED from healthy controls (HCs) by identified brain-basedcharacteristics. Resting-state functional magnetic resonance imaging data were acquired from 45 pED patients and 43 HCs. ⋯ This study identified altered regional activity and FC in specific brain regions of pED patients, which might be related to the development of pED. The application of machine learning confirmed the distinctive characteristics of these functional changes in the brain. The high accuracy of our diagnostic model suggested a promising direction for developing objective diagnostic tools for psychological disorders.
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Major depressive disorder (MDD) is a complex neuropsychiatric disorder potentially influenced by factors such as stress and inflammation. Chronic stress can lead to maladaptive brain changes that may trigger immune hyperactivation, contributing to MDD's pathogenesis. While the involvement of inflammation in MDD is well established, the effects of inflammatory preconditioning in animals subsequently exposed to chronic stress remain unclear. ⋯ A trend toward elevated IL-17 levels was also observed at the peripheral level. These findings indicate that inflammatory preconditioning contributes significantly to behaviors phenotypically associated with MDD. Furthermore, the study suggests that these behavioral changes are linked to a dysfunctional immune response and impaired neuroplasticity.
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The experiment was designed to explore the effects and mechanism of Dilong on alleviating cyclophosphamide (CTX)-induced brain injury in mice. Fifty male SPF Kunming mice aged 6-8 weeks were randomly divided into five groups: Group A served as the control group; Group B received intraperitoneal injection of CTX; Groups C, D, and E were administered Dilong at doses of 100, 200, and 400 mg/kg respectively for 14 days after intraperitoneal injection of CTX. Results showed that after modeling, the movement speed of mice significantly decreased (P < 0.05), and the number of neurons in the hippocampus and cortex decreased. ⋯ Dilong significantly increased mitochondrial respiratory enzyme activity (P < 0.05), and the mitochondrial structure was restored to some extent. By significantly reducing NLRP3/TLR4/caspase1/pro caspase1/GSDMD (P < 0.05), it increased neuronal cell survival. This resulted in an increase in neuronal cell survival, thus exerting a protective effect on the brain.