Uddin, Md Sahab Kabir, Md Tanvir Jalouli, Maroua Rahman, Md Ataur Jeandet, Philippe Behl, Tapan Alexiou, Athanasios Albadrani, Ghadeer M. Abdel-Daim, Mohamed M. Perveen, Asma Ashraf, Ghulam Md 2024-01-19T13:01:12Z 2024-01-19T13:01:12Z 2022-04-05 2022-01 1570-159X https://pubs.kist.re.kr/handle/201004/115821 Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the formation of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment but also strongly interacts with immunological processes in the brain. On the other hand, aggregated and misfolded proteins can bind with pattern recognition receptors located on astroglia and microglia and can, in turn, induce an innate immune response, characterized by the release of inflammatory mediators, ultimately playing a role in both the severity and the progression of the disease. It has been reported by genome-wide analysis that several genes which elevate the risk for sporadic AD encode for factors controlling the inflammatory response and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of external factors which may interfere with the immunological mechanisms of the brain and can induce disease progression. In this review, we discussed the mechanisms and essential role of inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune processes and modulation of risk factors may lead to future therapeutic or preventive AD approaches. English Bentham Science Publishers Neuroinflammatory Signaling in the Pathogenesis of Alzheimer's Disease Article 10.2174/1570159X19666210826130210 1 Current Neuropharmacology, v.20, no.1, pp.126 - 146 Current Neuropharmacology 20 1 126 146 N scie scopus 000754263700011 2-s2.0-85123813939 Neurosciences Pharmacology & Pharmacy Neurosciences & Neurology Pharmacology & Pharmacy Review MILD COGNITIVE IMPAIRMENT GENOME-WIDE ASSOCIATION TRANSGENIC MOUSE MODEL MICROGLIAL ACTIVATION OXIDATIVE STRESS TAU PATHOLOGY NF-KAPPA-B NECROSIS-FACTOR-ALPHA BETA-AMYLOID PROTEIN PRO-INFLAMMATORY CYTOKINES Neuroinflammation Alzheimer&apos s disease inflammatory cytokine astroglia microglia disease-associated microglia