Publications by authors named "Junqiang Yan"

Introduction: Autoimmune encephalitis is a neurological disease caused by abnormal autoimmune mechanisms, characterized by a range of symptoms such as psychiatric and behavioral abnormalities, cognitive impairment, memory decline, and seizures. It is primarily identified by the presence of autoantibodies against neuronal surface antigens in the cerebrospinal fluid. This disease is relatively rare in clinical settings, and its diagnosis remains challenging, with fewer than a hundred cases reported to date.

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Mesenchymal stem cell-derived extracellular vesicles, as carriers for intercellular communication, are rich in bioactive substances such as proteins and nucleic acids, and show unique potential in the treatment of neurodegenerative diseases. Their vesicular structure, with a diameter of 30-150 nm, can penetrate the blood-brain barrier and modulate the activity of microglia and astrocytes by delivering functional molecules. This process inhibits the release of pro-inflammatory factors and enhances the expression of anti-inflammatory mediators, thereby alleviating neuroinflammation in the pathological process of neurodegenerative diseases.

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Menstrual-related migraine (MRM) is a neurovascular disorder associated with decreased sex hormone levels. The menstrual cycle influences both cerebrovascular function and functional brain connectivity, with accumulating evidence linking migraine to altered connectivity, particularly in the insula. However, the neuropathological mechanisms underlying MRM during the menstrual cycle remain poorly understood.

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Background: Autoimmune diseases comprise a spectrum of illnesses stemming from a common etiology: the loss of self-tolerance. The organ crucial for the establishment and maintenance of central and peripheral tolerance, namely the thymus, has rarely been explored across these diseases.

Methods: In a multicentre radiological case-control study, we characterized the thymus in 16 prevalent autoimmune diseases using chest computed tomography (CT) images from patients and age- and sex-1:1 matched healthy controls.

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Objective: The association of B lymphocytes and B lymphocyte subsets and Parkinson's disease (PD) is increasingly acknowledged. However, there is inconsistence in the alterations of B lymphocytes or B lymphocyte subsets in peripheral blood of PD patients. To comprehensively understand its changes in PD patients,it is necessary to conduct a systematic review on this subject.

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Patent foramen ovale (PFO) is one of the main causes of ischemic stroke. Due to the complex characteristics of contrast transthoracic echocardiography (cTTE), PFO classification is time-consuming and laborious in clinical practice. For this reason, a variety of PFO diagnostic models have been presented based on machine learning in recent years.

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For diverse neurodegenerative disorders, microglial cells are activated. Furthermore, dysfunctional and hyperactivated microglia initiate mitochondrial autophagy, oxidative stress, and pathological protein accumulation, ending with neuroinflammation that exacerbates damage to dopaminergic neurons and contributes significantly to the pathology of neurodegenerative disorder. Microglial over-activation is closely associated with the secretion of pro-inflammatory cytokines, the phagocytosis of injured neurons, and the modulation of neurotoxic environments.

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This review elucidates the pivotal role of pyroptosis, triggered by gut microbiota, in the development of multiple sclerosis (MS), emphasizing its significance within the gut-brain axis. Our comprehensive analysis of recent literature reveals how dysbiosis in the gut microbiota of MS patients-characterized by reduced microbial diversity and shifts in bacterial populations-profoundly impacts immune regulation and the integrity of the central nervous system (CNS). Pyroptosis, an inflammatory form of programmed cell death, significantly exacerbates MS by promoting the release of inflammatory cytokines and causing substantial damage to CNS tissues.

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Alpha-synuclein (α-syn) is a major pathological marker of Parkinson's disease (PD), and its abnormal expression and aggregation lead to dopaminergic neuron degeneration, in which oxidative stress plays an important role. However, the exact molecular mechanism by which α-syn causes PD remains unclear. In this study, exogenous α-syn, also known as α-syn preformed fibrils (α-syn PFFs), was used to construct in vivo and in vitro models of PD.

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Regulated cell death (such as apoptosis, necroptosis, pyroptosis, autophagy, cuproptosis, ferroptosis, disulfidptosis) involves complex signaling pathways and molecular effectors, and has been proven to be an important regulatory mechanism for regulating neuronal aging and death. However, excessive activation of regulated cell death may lead to the progression of aging-related diseases. This review summarizes recent advances in the understanding of seven forms of regulated cell death in age-related diseases.

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Chinese medicine is a unique and complex medical system with complete and rich scientific theories. The textual data of Traditional Chinese Medicine (TCM) contains a large amount of relevant knowledge in the field of TCM, which can serve as guidance for accurate disease diagnosis as well as efficient disease prevention and treatment. Existing TCM texts are disorganized and lack a uniform standard.

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Parkinson's disease (PD) is characterized by the progressive death of dopamine (DA) neurons and the pathological accumulation of α-synuclein (α-syn) fibrils. In our previous study, simulated PHB2 phosphorylation was utilized to clarify the regulatory role of c-Abl in PHB2-mediated mitophagy in PD models. In this investigation, we employed an independently patented PHB2Y121 phosphorylated antibody in the PD model to further verify that the c-Abl inhibitor STI571 can impede PHB2Y121 phosphorylation, decrease the formation of α-Syn polymers, and improve autophagic levels.

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Article Synopsis
  • Endoplasmic reticulum stress and mitochondrial dysfunction are crucial in Parkinson's disease, but how they interact is still not well understood.
  • This study investigates the role of Prohibitin-2 (PHB2), an autophagy receptor in mitochondria, and its relationship with the protein Parkin and the endoplasmic reticulum stress regulator PERK in the context of Parkinson's disease.
  • Using mouse and cell models of Parkinson's disease, the research found that loss of PHB2 worsens neuron damage and motor functions, while overexpression of PHB2 and Parkin promotes mitophagy, indicating that PHB2 may influence disease progression through its interactions with PERK and Parkin.
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Aberrant innate immunity in the brain has been implicated in the pathogenesis of several central nervous system (CNS) disorders, including Alzheimer's disease, Huntington's disease, Parkinson's disease, stroke, amyotrophic lateral sclerosis, and depression. Except for extraparenchymal CNS-associated macrophages, which predominantly afford protection against peripheral invading pathogens, it has been reported that microglia, a population of macrophage-like cells governing CNS immune defense in nearly all neurological diseases, are the main CNS resident immune cells. Although microglia have been recognized as the most important source of reactive oxygen species (ROS) in the CNS, ROS also may underlie microglial functions, especially M1 polarization, by modulating redox-sensitive signaling pathways.

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Menstrually-related migraine (MM) is a primary migraine in women of reproductive age. The underlying neural mechanism of MM was still unclear. In this study, we aimed to reveal the case-control differences in network integration and segregation for the morphometric similarity network of MM.

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Oxidative stress plays a crucial role in the occurrence and development of Parkinson's disease (PD). Rutin, a natural botanical ingredient, has been shown to have antioxidant properties. Therefore, the aim of this study was to investigate the neuroprotective effects of rutin on PD and the underlying mechanisms.

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Oxidative stress plays a key role in cerebral ischemia/reperfusion injury. Artemisinin (ART) has antioxidative stress activity in addition to its powerful antimalarial effects. In this article, we investigated the effect of ART on OGD/R-induced oxidative stress injury and its underlying mechanisms.

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Mitophagy and oxidative stress play important roles in Parkinson's disease (PD). Dysregulated mitophagy exacerbates mitochondrial oxidative damage; however, the regulatory mechanism of mitophagy is unclear. Here, we provide a potential mechanistic link between c-Abl, a nonreceptor tyrosine kinase, and mitophagy in PD progression.

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Objective: The efficacy of melatonin on sleep disorders in Parkinson's disease (PD) is still unclear. The purpose of this study was to investigate the efficacy of melatonin on sleep disorders in PD by summarizing evidence from randomized clinical trials (RCTs).

Methods: PubMed, Cochrane Library, EMBASE, and Web of Science databases were searched for studies published before 20 August 2021.

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The progression of Parkinson's disease (PD) is often accompanied by the loss of substantia nigra dopaminergic neurons, mitophagy damage, learning, and memory impairment. Idebenone is a therapeutic drug that targets the mitochondria of neurodegenerative diseases, but its role in Parkinson's disease and its pathological mechanism are still unclear. The purpose of this study was to investigate whether idebenone could improve behavioral disorders, especially motor, learning, and memory disorders, in mouse PD models and to explore its molecular mechanism.

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Background: Ferroptosis is an autophagy-dependent form of cell death, sometimes called "ferritinophagy". Its related pathway has been proven to regulate the programmed death of glioma stem cells. Mining autophagy-dependent ferroptosis-related gene (AD-FRG) signature could facilitate the discovery of mechanisms and therapeutic targets showing drug resistance to chemotherapeutic drugs.

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BACKGROUND Non-visual effects of the retina have been increasingly confirmed in developing Parkinson disease (PD). Light therapy (LT) has been proven to be an effective non-pharmacotherapy for improving the prognosis of PD, but the pathway of action is unclear, and there is a lack of a unified and standardized LT regimen. We aimed to evaluate the efficacy and safety of various LT measures in improving motor and non-motor symptoms in patients with idiopathic PD via a meta-analysis.

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The effects of rotigotine transdermal patch (RTG) on the neuropsychiatric symptoms of Parkinson's disease (PD) outcomes remain controversial. The aim of this review was to determine the efficacy and safety of RTG on the neuropsychiatric symptoms of PD. In this systematic review and meta-analysis, PubMed, Cochrane Library, EMBASE, and Web of Science were searched for randomized controlled trials comparing RTG and placebo in PD up to May 10, 2021.

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To review the therapeutic effects of drugs on REM sleep behavior disorder (RBD) in Parkinson's disease (PD) by searching the MEDLINE/PubMed, Embase, Cochrane, and CBM databases. According to the inclusion and exclusion criteria, studies were included after excluding duplicate data. We evaluated the safety and efficacy of pharmacological intervention to improve RBD in patients with Parkinson's disease (PD-RBD).

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Background: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects.

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