Copyright © 2026 Authors retain the copyright of this article. This article is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

@article{180329,
        author = {Simham Sudhakar and Dr.M.Madhu and U.Narasimhulu and Dr.K.Adinarayana},
        title = {The role of neuroinflammation in alzheimers disease progression},
        journal = {International Journal of Innovative Research in Technology},
        year = {2025},
        volume = {12},
        number = {1},
        pages = {2093-2104},
        issn = {2349-6002},
        url = {https://ijirt.org/article?manuscript=180329},
        abstract = {Alzheimer's disease (AD) is a progressive 
neurological disorder characterized by deficits in 
memory, cognition, behavior, and personality. 
Neuroinflammation 
significantly 
affects 
AD 
progression, with immune cells such as microglia and 
astrocytes playing crucial roles. Activated microglia 
release inflammatory molecules that can potentially 
initiate chronic inflammation. Astrocyte activation 
varies by brain region and disease stage and sometimes 
precedes microglial activation. Inflammatory proteins, 
including interleukins and tumor necrosis factor-alpha, 
promote inflammatory pathways and, with other 
molecules, induce neuronal death. The activation of the 
complement system in AD can contribute to and 
mitigate disease progression. The key features of AD 
include amyloid-beta accumulation, plaque formation, 
excessive tau protein phosphorylation, neurofibrillary 
tangle development, and synaptic impairment and loss, 
all of which are influenced by neuroinflammation. 
Initial neuroinflammation may be protective; however, 
prolonged inflammation exacerbates the disease. 
Potential therapies include anti-inflammatory drugs, 
immune system modulation, and treatments targeting 
microglia and astrocytes. Studying neuroinflammation 
in AD is challenging because of the complex immune 
response of the brain, limitations of animal models, and 
difficulties in translating the findings to humans. 
Emerging research on novel biomarkers, personalized 
medicine, and combination therapies targeting multiple 
aspects of neuroinflammation may lead to more 
effective prevention and treatment strategies for AD.},
        keywords = {Alzheimer's disease, Neuroinflammation,  Microglia, Astrocytes, Neurodegeneration, Cytokines,  Amyloid-beta},
        month = {June},
        }