NEUROINFLAMMATION AND ALZHEIMER'S DISEASE-AN EMERGING TARGET FOR DISEASE-MODIFYING THERAPIES: META-ANALYSIS

Abstract

AD stands as the prime reason for dementia because it causes decreasing cognitive abilities which manifests as memory troubles alongside diminished capability to manage daily tasks. Current AD research priority now centers on neuroinflammation as a significant factor that accelerates disease progression even though past theories mainly focused on amyloid-beta (Aβ) plaques and tau protein tangles. Glial cell activation particularly microglia and astrocyte activation through neuroinflammation leads to neuronal damage while causing cognitive impairment in AD patients. AD patients demonstrate elevated inflammatory cytokines like IL-6, TNF-α, CRP which signal a prolonged inflammatory state that worsens neurodegenerative damage in the brain. AD pathophysiology relies on the function of NLRP3 inflammasome molecular pathways alongside NF-κB signaling and microglial TREM2 receptors. A meta-analysis of systematic studies analyzes the effects of neuroinflammatory markers on disease worsening while examining therapeutic outcomes of anti-inflammatory treatment methods. This analysis reviewed studies from 2015 to 2024 which followed systematic criteria that included clinical trials and randomized controlled trials (RCTs) and cohort studies that investigated both neuroinflammatory biomarkers and therapeutic interventions. Research findings demonstrate an established relationship where higher levels of CRP and IL-6 connect to increased cognitive deterioration rates. The review examines anti-inflammatory drug strategies like NSAIDs and monoclonal antibodies for therapeutic use but existing clinical evidence lacks definitive proof. Neuroinflammation presents important opportunities for AD therapy according to this review yet additional research about early detection biomarkers and disease-altering treatments must continue.