EXPLORING THE MECHANISMS OF NEUROINFLAMMATION IN THE PATHOGENESIS OF NEURODEGENERATIVE DISEASES

Abstract

Neuroinflammation has emerged as a critical factor in the pathogenesis of neurodegenerative diseases (NDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). This study investigates the mechanisms underlying neuroinflammation and its role in disease progression, with a focus on glial cell activation, the inflammasome, and the blood-brain barrier (BBB). In vitro experiments utilizing microglial and astrocyte cell lines exposed to amyloid-beta (Aβ) peptides and alpha-synuclein aggregates revealed a significant increase in pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), as well as oxidative stress and a reduction in cell viability. In vivo, transgenic mouse models of AD and PD exhibited impaired cognitive and motor function, corroborating the neuroinflammatory response observed in vitro. The research showed enhanced activation of microglia and astrocytes through elevated Iba-1 and GFAP expression in these animals using immunohistochemical analysis.  A computational evaluation of RNA-sequencing human brain tissue data in neurodegenerative illnesses showed that inflammatory pathways included NF-kB and NLRP3 inflammasome.  The research shows neuroinflammation functions through intricate mechanisms to advance disease establishment and indicates therapy approaches focusing on glial activation and inflammatory networks could help minimize neurodegenerative disease effects.  This research reveals important information about neuroinflammation as a therapeutic target in AD and PD treatment and shows all the molecular pathways involved in the disease process.