Neuroinflammation: The Pathogenic Mechanism of Neurological Disorders

• Published in: International journal of molecular sciences Vol. 23; no. 10; p. 5744
• Main Author: Gorji, Ali
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 20.05.2022; MDPI
• Subjects: Animal cognition; Conflicts of interest; Cytokines; Epilepsy; Immune system; Infections; Inflammation; MicroRNAs; Multiple sclerosis; Nervous system; Neurodegeneration; Neurological disorders; Oxidative stress; Spinal cord injuries; Trauma; Traumatic brain injury; Tumor necrosis factor-TNF
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23105744

Neuroinflammation is the innate and adaptive immune responses that are initiated toward a variety of harmful insults (such as infection, ischemia, stress, and trauma) through the release of inflammatory mediators (such as cytokines, chemokines, and reactive oxygen species) by various immune cells (like microglia, astrocytes, peripherally derived immune cells, and endothelial cells) [2]. Neuroinflammation in the initial stage is mainly beneficial and protective; however, evidence from both clinical and experimental studies indicates that prolonged or excessive inflammation is a pivotal pathological driver of several neurological disorders, such as cerebrovascular diseases (CVD), traumatic brain and spinal cord injuries, neurodegenerative diseases, epilepsy, multiple sclerosis (MS), psychological disorders, and chronic pain. Based on the evidence of a potential correlation between stress-induced inflammation and epilepsy, Espinosa-Garcia and colleagues have described the importance of early interventions for both acute and chronic stress in the improvement of diagnosis, therapy, and outcomes for patients with epilepsy, particularly for subjects with psychiatric comorbidities [10]. [...]modulation of inflammatory processes and mediators represent relevant potential targets for the treatment of epilepsy [11]. In this issue, Aboghazale and colleagues evaluated the electrophysiological alterations of rat brain after traumatic brain injury and have shown the occurrence of both SD and SD-induced depression of cortical activity. [...]their findings revealed that while the occurrence of SD following closed brain trauma led to enhanced oxidative stress (elevated reactive oxygen species), traumatic brains exhibited a decreased antioxidant defense (downregulation of mRNA expression of antioxidant enzymes in response to oxidative stress) [29].