Influence of microglia and astrocyte activation in the neuroinflammatory pathogenesis of Alzheimer's disease: Rational insights for the therapeutic approaches. (January 2019)

• Record Type: Journal Article
• Authors: Ahmad, Mir Hilal; Fatima, Mahino; Mondal, Amal Chandra
• Is Part Of: Journal of clinical neuroscience. Volume 59(2019)
• Page Start: 6
• Page End: 11
• Publication Date: 2019-01
• Subjects: Alzheimer's disease -- Neuroinflammation -- Cytokines -- Microglia -- Astrocytes; Brain -- Surgery -- Periodicals; Neurosciences -- Periodicals; Nervous system -- Surgery -- Periodicals; Brain -- surgery -- Periodicals; Neurosurgical Procedures -- Periodicals; Neurosciences -- Periodicals; Electronic journals; 616.8
• DOI: 10.1016/j.jocn.2018.10.034
• Languages: English
• ISSNs: 0967-5868

Abstract

Highlights: In AD, the inflammatory response is mainly located to the vicinity of Aβ-plaques. Aβ-plaques deposition causes chronic activation of the immune system. Persistent activation of astrocytes and microglia result in neuroinflammation during AD. Neuroinflammation during AD serves to exacerbate AD progression. Abstract: Alzheimer's disease (AD), the most common progressive neurodegenerative disorder is characterized by the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles (NFTs). Increasing evidences suggest a link between neuroinflammation and neuronal dysfunction in AD, orchestrated by the progressive activation of microglial cells and astrocytes with the consequent overproduction of proinflammatory molecules. The concomitant release of anti-inflammatory mediators antagonizes the inflammatory processes and leading to the severity of the AD pathology. The simultaneous detection of these inflammatory molecules in the pre-symptomatic stage may help in the early diagnosis of the AD. We have discussed the impact of microglia and astrocytic cells, the principal agents in the neuroinflammation process, in relation to the progression of the AD. Modulation of the risk factors and targeting of these immune mechanisms could lead to better therapeutic or preventive strategies for the AD. Further studies need to determine, how the inhibition of inflammatory factors could be used for the AD alternative therapies.