Search Results (2)

Binge or chronic alcohol consumption causes neuroinflammation and leads to alcohol use disorder (AUD). AUD not only affects the central nervous system (CNS) but also leads to pathologies in the peripheral and enteric nervous systems (ENS). Thus, understanding the mechanism of the immune signaling to target the effector molecules in the signaling pathway is necessary to alleviate AUD. Growing evidence shows that excessive alcohol consumption can activate neuroimmune cells, including microglia, and change the status of neurotransmitters, affecting the neuroimmune system. Microglia, like peripheral macrophages, are an integral part of the immune defense and represent the reticuloendothelial system in the CNS. Microglia constantly survey the CNS to scavenge the neuronal debris. These cells also protect parenchymal cells in the brain and spinal cord by repairing nerve circuits to keep the nervous system healthy against infectious and stress-derived agents. In an activated state, they become highly dynamic and mobile and can modulate the levels of neurotransmitters in the CNS. In several ways, microglia, enteric glial cells, and macrophages are similar in terms of causing inflammation. Microglia also express most of the receptors that are constitutively present in macrophages. Several receptors on microglia respond to the inflammatory signals that arise from danger-associated molecular patterns (DAMPs), pathogen-associated molecular patterns (PAMPs), endotoxins (e.g., lipopolysaccharides), and stress-causing molecules (e.g., alcohol). Therefore, this review article presents the latest findings, describing the roles of microglia and enteric glial cells in the brain and gut, respectively, and their association with neurotransmitters, neurotrophic factors, and receptors under the influence of binge and chronic alcohol use, and AUD. Full article

Coronavirus 2019 (COVID-19) is an infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that mainly affects the lungs. COVID-19 symptoms include the presence of fevers, dry coughs, fatigue, sore throat, headaches, diarrhea, and a loss of taste or smell. However, it is understood that SARS-CoV-2 is neurotoxic and neuro-invasive and could enter the central nervous system (CNS) via the hematogenous route or via the peripheral nerve route and causes encephalitis, encephalopathy, and acute disseminated encephalomyelitis (ADEM) in COVID-19 patients. This review discusses the possibility of SARS-CoV-2-mediated Multiple Sclerosis (MS) development in the future, comparable to the surge in Parkinson’s disease cases following the Spanish Flu in 1918. Moreover, the SARS-CoV-2 infection is associated with a cytokine storm. This review highlights the impact of these modulated cytokines on glial cell interactions within the CNS and their role in potentially prompting MS development as a secondary disease by SARS-CoV-2. SARS-CoV-2 is neurotropic and could interfere with various functions of neurons leading to MS development. The influence of neuroinflammation, microglia phagocytotic capabilities, as well as hypoxia-mediated mitochondrial dysfunction and neurodegeneration, are mechanisms that may ultimately trigger MS development. Full article