2Introduction: Spreading Depression (SD) is a pathophysiological phenomenon that occurs as a transient wave of depolarization of neurons and glial cells, and results in a temporary suppression of the activity of neurons. In this phenomenon, there is a disturbance in the distribution and balance of ions between the extracellular and intracellular environments and in cellular metabolism. Furthermore, SD is accompanied by a short increase in bioelectrical activity, followed by a strong transient depression of neuronal activity and a long-term excitability of the neuronal network. Recently, the Neuroinflammatory function of this phenomenon, as one of the main contributors to neurological Diseases, has been widely investigated. The role of SD has been revealed in some neurological Diseases, such as migraine with aura, epilepsy, transient global amnesia, and cerebrovascular Diseases, including cerebral ischemia-infarction and stroke, as well as intracranial hemorrhage caused by traumatic head injury. Conclusion: Despite the large and growing body of evidence, the exact mechanism of SD propagation is still not clear and requires more in-depth investigations. Therefore, in this review, we discuss the underlying mechanism of SD and highlight the role of SD in the development of Neuroinflammatory Diseases.

Introduction: The proper development and function of the central nervous system (CNS) depends fundamentally on the activity of parenchymal sentinels called microglia. Microglia currently have the greatest ability and capability compared to other cells in the CNS, with the capacity to adapt morphologically and functionally to their changing environment. Even at rest, microglia cells are highly dynamic and constantly survey the condition in the CNS. Following injury, these cells rapidly change morphology and migrate towards the site of injury. Any injury to the CNS is accompanied by the release of mediators that serve as signals for the activation or chemotaxis of microglia. They can communicate with neurons, astrocytes, and other cells of the immune system through a large number of signaling pathways. Microglia are critical contributors to the homeostasis of the CNS and dysregulation of these cells contributes to the pathophysiology of neurodegenerative Diseases. Conclusion: microglia are crucial to maintaining CNS homeostasis through their dynamic rapid response to insults. Their ability to interact with various cell types and adapt to environmental changes points to their important role in CNS pathologies, including brain tumors, and neurodegenerative Diseases such as Parkinson's disease, Alzheimer's disease, and Amyotrophic lateral sclerosis.

Dear Editor, At the beginning of 2020, first COVID-19 cases were reported outside China. SARS-CoV-2 presents a marked inflammatory response, which causes the cytokine storm, a state of self-sustained hyperinflammation that occurs together with a poor immune system (1, 2). At the brain level, neural and immune cells serve as reservoirs for the virus, thereby allowing neurodegenerative development (3, 4). . .

Most patients with X-linked agammaglobulinemia are susceptible to infections, while some cases also suffer from inflammatory or autoimmune complications. We describe a patient with progressive encephalitis who improved after the use of immunomodulatory treatment with corticosteroids, fluoxetine, and nitazoxanide. In most of the cases the evolution of the progressive encephalitis is complicated and catastrophic. Based on our experience and the review of the literature, we propose the use of this combined treatment to control this devastating complication.

Introduction: Alzheimer's disease (AD), one of the most common forms of dementia, has become a significant public health challenge. Given the rising prevalence of this disease, innovative research is exploring complex connections that could lead to a better understanding and treatment of AD. One such research area involves examining the impact of the gut microbiome on brain health, particularly its influence on AD. Recent studies have demonstrated a strong connection between the gut microbiome and AD, highlighting the potential for significant advancements in prevention and treatment. Conclusion: Recent studies suggest that changes in the composition of the gut microbiome may be associated with the progression of AD. Particularly, several investigations indicate that probiotics and certain diets can reduce brain inflammation and improve cognitive functioning in AD patients. These findings point to the importance of further investigating the relationship between the microbiome and AD. This could lead to the development of novel prevention and treatment methods.

Background: Inflammation plays a major part in brain ischemia. Propolis is a polyphenol-rich hive product with a set of pharmaceutical properties. Objectives: This research aims to investigate the impact of water extracts of brown propolis (WEPs) on stroke outcomes and inflammatory responses in a rat model of permanent middle cerebral artery occlusion (MCAO). Materials & Methods: This experimental study was conducted in Rafsanjan, Iran, in 2017. WEPs were experimentally prepared from two regions in Iran. Gas chromatography–, mass spectrometry and Folin–, Ciocalteu assays were used to determine chemical portrayal and the total polyphenol content, respectively. A total of 66 male adult mice were divided randomly into the surgical sham, control (vehicle-treated), and four WEPs-treated animal groups. WEPs-treated groups received doses of 100 and 200 (mg/kg, IP) four times, and their behavioral tests, brain edema, infarct volume, and tumor necrosis factor-alpha (TNF-α, ) level were evaluated. Results: The samples were not significantly different in terms of the concentration of the total polyphenol content. Compared to the control, WEPs led to a substantial decrease in the TNF-α,level (P<0. 05) as well as a subsequent reduction in the brain edema and infarct volume (P<0. 001) in all treatment groups. Furthermore, there was a significant improvement in neurological deficits and sensory-motor impairments level (P<0. 05). Conclusion: According to the study findings, WEPs reduce brain ischemia damage, perhaps by exerting a neuroprotective effect on stroke-induced Neuroinflammatory responses.

Introduction: Despite substantial advances in clinical care, spinal cord injuries and their associated persistent complications remain an incurable condition, with devastating physical and psychological consequences for patients and caregivers. Clinical diagnosis of spinal cord injuries is mainly based on the neurological deficits. In recent years, imaging techniques have been used to evaluate acute spinal cord injuries. However, in many centers, advanced imaging techniques are not available, or the patient's unstable condition limits using advance approaches. Since reliable prediction of recovery in the acute phase is crucial for selecting appropriate neuroprotective treatment, ‪there is an urgent need to identify and implement new methods for more accurate prediction and planning to reduce permanent complications. Identifying biomarkers to predict spinal cord injury helps the management of injured patients and supports accurate diagnosis and treatment. Some proteins have been identified as promising biomarkers for central nervous system injury, both in cerebrospinal fluid (CSF) and blood serum. This review aims to evaluate the diagnostic and prognostic roles of these proteins and neurostructural biomarkers in spinal cord injury. Conclusion: The identification of biochemical biomarkers is becoming increasingly valuable in the management of spinal cord injury. These markers have significant potential to assess the severity of primary injury objectively, predict neurological outcome, and monitor recovery and secondary complications. Studies show that biomarker levels in blood serum and CSF correlate with injury severity as measured by standardized clinical scales and can distinguish between patients with good and poor prognoses. Due to the limited accessibility and invasive nature of CSF sampling, research has increasingly focused on identifying reliable serum-based biomarkers. Furthermore, the distinct temporal dynamics of biomarker expression in the acute phase (reflecting primary injury) versus the chronic phase (influenced by systemic complications) highlight the need to define specific markers appropriate to each stage.