Clinical and Experimental Neuroimmunology最新文献

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to hallmark motor symptoms such as bradykinesia, tremors, and rigidity. Emerging evidence suggests that the dysregulation or aberrant expression of long noncoding RNAs (lncRNAs) plays a critical role in the pathogenesis of PD by activating the inflammasome, either directly or via oxidative stress. Aberrant lncRNA expression has been linked to alterations in genes related to oxidative stress, causing an imbalance between reactive oxygen species (ROS) and antioxidant defenses. This imbalance contributes to mitochondrial dysfunction and neuronal damage. The NLRP3 inflammasome is a multiprotein complex comprising a sensor protein (eg, NLRP3), an adaptor protein (ASC), and an effector protein (caspase-1). Its activation involves priming via NF-κB signaling and is triggered by ROS, mitochondrial dysfunction, death-associated molecular patterns, or extracellular ATP. Once activated, the inflammasome promotes the cleavage and maturation of the proinflammatory cytokines IL-1β and IL-18, amplifying neuroinflammation and leading to neurodegeneration in PD. Crosstalk between dysregulated lncRNAs, ROS production, and inflammasome activation creates a vicious cycle of neuroinflammation and neurodegeneration, exacerbating PD progression. This review explores the molecular mechanisms linking lncRNA dysregulation to inflammasome activation in PD, either directly or through oxidative stress. It also highlights key lncRNAs involved in these processes. Furthermore, potential therapeutic strategies targeting these pathways, such as antioxidants, lncRNA modulators, and inflammasome inhibitors, offer promising avenues to mitigate neuroinflammation and slow neurodegeneration in PD.

Inflammatory myopathy is classified into primary autoimmune myositis and secondary myositis due to various factors, such as drugs and autoimmune connective tissue diseases. Autoimmune myositis mainly consists of dermatomyositis, antisynthetase syndrome-associated myositis, immune-mediated necrotizing myopathy, and inclusion body myositis. This review aims to provide insights into muscle pathology for clinical practice and an understanding of pathophysiology in inflammatory myopathy by summarizing current knowledge about the pathology of each subform of autoimmune myositis and some secondary myositis. Dermatomyositis is associated with type I interferon upregulation. Expression of myxovirus resistance protein A (a type I interferon-induced protein) in myofibers is utilized as a sensitive diagnostic marker. Antisynthetase syndrome-associated myositis is morphologically characterized by perifascicular necrosis. A recent study suggests the presence of a characteristic immunological micromilieu suitable for plasma cells in the skeletal muscle tissue. Immune-mediated necrotizing myopathy features an active necrotic and regenerating process. In inclusion body myositis, inflammatory cellular infiltration and rimmed vacuoles reflecting autophagy disruption are observed. The lymphocytes invading myofibers are composed of a highly differentiated T-cell population, which is considered a potential therapeutic target.

The progression of intracranial aneurysm lesions involves complex mechanisms influenced by various factors, including inflammation, oxidative stress and endothelial dysfunction. This comprehensive review delves into the intricate interplay between specific dietary patterns and the progression of intracranial aneurysm lesions. Understanding the impact of these dietary factors on inflammation, oxidative stress and endothelial dysfunction offers valuable insights into noninvasive strategies for managing intracranial aneurysm progression, addressing a critical gap in current therapeutic approaches.