Neuroscience
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Ischemic stroke can cause damage to neurons, resulting in neurological dysfunction. The main treatments in the acute phase include intravenous thrombolysis, endovascular stent-assisted vascular thrombectomy and antiplatelet therapy. Due to the limitations of the time window and the risk of early intracranial hemorrhage, finding active treatment plans is crucial for improving therapy. ⋯ This tolerance, induced by stressors like ischemia and hypoxia, can become an effective and convenient treatment approach for ischemic stroke. The molecular mechanisms involved in preconditioning are extremely complex. This article focuses on the main preconditioning treatment methods for ischemic stroke, discusses the specific molecular mechanisms of different treatment methods, and explores their action pathways and effects on corresponding target cells, thus opening up a brand-new direction for the treatment strategies of ischemic stroke.
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Review
MicroRNAs in Parkinson's disease: From pathogenesis to diagnostics and therapeutic strategies.
Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by pathological changes, including the loss of dopaminergic neurons and abnormal aggregation of α-synuclein (α-syn). Certain cellular and molecular events are involved; however, the origin and significance of these events remain uncertain. The discovery of microRNAs (miRNAs) predicted to play a pivotal role in various regulatory processes has emerged. ⋯ This review aims to encapsulate recent research developments concerning the function of miRNAs in the pathophysiology of PD and their prospective applications as diagnostic and therapeutic biomarkers, targets, and pharmaceuticals. The most effective drug delivery approach for the treatment of PD, transnasal-cerebral drug delivery, has also been briefly described. The advantage of this delivery strategy is its capacity to bypass the blood-brain barrier, enabling direct administration of medication to the brain, which improves therapeutic efficacy and minimizes side effects.
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Maintaining balance while simultaneously performing other tasks is common during everyday activities. However, this dual-tasking (DT) divides attention and increases cognitive demand, which can be detrimental to stability in older adults. It is unknown if the focus of attention influences how a dual-task affects balance and whether this is detectable in middle-aged adults. ⋯ COP excursion was also greater when attention was 'fixed' and was consistently larger in MA. MA drove a positive correlation between PFC activity and COP excursion during DT indicative of a higher attentional demand during distraction. Taken together, this study suggests that PFC processing and posture control are different in middle aged adults compared to young adults.
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In addition to nasal symptoms, allergic rhinitis (AR) has increasingly been reported to be associated with depression-like behaviors. Recent evidence suggests that neuroinflammation in the hypothalamus may cause these depressive symptoms in AR. However, the precise mechanisms and effective treatments remain to be elucidated. ⋯ Increased TRPV1 expression activates the NLRP3 inflammasome in hypothalamic microglia, promoting the pathological process of depressive-like behavior in AR mice. Metformin could effectively treat neuroinflammation by regulating microglia via TRPV1 downregulation, indicating its potential as a treatment for depressive-like behaviors in AR.
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There is mounting evidence for the involvement of the immune system, neuroinflammation and disturbed gut microbiota, or dysbiosis, in attentive-deficit/hyperactivity disorder (ADHD). Gut dysbiosis is strongly implicated in many physical, autoimmune, neurological, and neuropsychiatric conditions, however knowledge of its particular pathogenic role in ADHD is sparse. As such, this narrative review examines and synthesizes the available evidence related to inflammation, dysbiosis, and neural processes in ADHD. ⋯ Compositional differences of taxa important to key gut-brain axis pathways, in particular Bacteroides species and Faecalibacterium, may contribute to inflammation, brain functioning differences, and symptoms, in ADHD. We have identified one possible model of ADHD etiopathogenesis involving systemic inflammation, an impaired blood-brain barrier, and neural disturbances as downstream consequences of gut dysbiosis. Nevertheless, studies conducted to date have varied degrees of methodological rigour and involve diverse participant characteristics and analytical techniques, highlighting a need for additional research.