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Updated: Jun 25, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Decoding the role of the CCL2/CCR2 axis in Alzheimer's disease and innovating therapeutic approaches: Keeping All
Reyhaneh Arfaei1, Narges Mikaeili1, Fatemeh Daj1
1Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Abstract:
Alzheimer's disease (AD), as a neurodegenerative disorder, distresses the elderly in large numbers and is characterized by β-amyloid (Aβ) accumulation, elevated tau protein levels, and chronic inflammation. The brain's immune system is aided by microglia and astrocytes, which produce chemokines and cytokines. Nevertheless, dysregulated expression can cause hyperinflammation and lead to neurodegeneration. CCL2/CCR2 chemokines are implicated in neurodegenerative diseases exacerbating. Inflicting damage on nerves and central nervous system (CNS) cells is the function of this axis, which recruits and migrates immune cells, including monocytes and macrophages. It has been shown that targeting the CCL2/CCR2 axis may be a therapeutic option for inflammatory diseases. Using the current knowledge about the involvement of the CCL2/CCR2 axis in the immunopathogenesis of AD, this comprehensive review synthesizes existing information. It also explores potential therapeutic options, including modulation of the CCL2/CCR2 axis as a possible strategy in AD.
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