The Role of Neuroinflammation in Alzheimer's Disease Progression: Mechanisms and Therapeutic Targets
*Corresponding Author: Marco Soy, Department of Psychiatry, Weill Cornell Medical College, New York, USA, Email: soymarco08090@gmail.comReceived Date: Jan 01, 2025 / Published Date: Jan 30, 2025
Citation: Marco S (2025) The Role of Neuroinflammation in Alzheimer’s DiseaseProgression: Mechanisms and Therapeutic Targets J Dement 9: 261.
Copyright: © 2025 Marco S. This is an open-access article distributed under theterms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author andsource are credited.

Abstract
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, memory impairment, and behavioral changes. Recent research highlights the role of neuroinflammation in AD progression. Inflammation in the brain, driven by glial cells, has been implicated in the initiation and exacerbation of AD pathology. Activated microglia and astrocytes release pro-inflammatory cytokines, which may exacerbate neuronal damage, synaptic dysfunction, and contribute to the deposition of amyloid-beta plaques and tau tangles, hallmarks of AD. This review examines the molecular mechanisms underlying neuroinflammation in AD, including the activation of inflammatory pathways such as the NF-kB and JAK/STAT pathways, and how they influence disease progression. Additionally, we explore potential therapeutic targets aimed at modulating neuroinflammation to slow AD progression. The therapeutic strategies discussed include anti-inflammatory agents, immune modulation, and nanomedicine approaches. Addressing neuroinflammation could provide new opportunities for AD treatment and potentially improve outcomes for affected individuals.