Cited by 120Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

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Mechanisms of Mononuclear Phagocyte Recruitment in Alzheimers Disease

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Hickman, Suzanne E., Khoury, Joseph El·2010·CNS & Neurological Disorders - Drug Targets

DOI 10.2174/187152710791011982PMC PMC3684802

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Abstract

Alzheimer's disease (AD) is associated with a significant neuroinflammatory component. Mononuclear phagocytes including monocytes and microglia are the principal cells involved, and they accumulate at perivascular sites of beta-amyloid (Abeta) deposition and in senile plaques. Recent evidence suggests that mononuclear phagocyte accumulation in the AD brain is dependent on chemokines. CCL2, a major monocyte chemokine, is upregulated in the AD brain. Interaction of CCL2 with its receptor CCR2 regulates mononuclear phagocyte accumulation in a mouse model of AD. CCR2 deficiency leads to lower mononuclear phagocyte accumulation and is associated with higher brain Abeta levels, specifically around blood vessels, suggesting that monocytes accumulate at sites of Abeta deposition in an initial attempt to clear these deposits and stop or delay their neurotoxic effects. Indeed, enhancing mononuclear phagocyte accumulation delays progression of AD. Here we review the mechanisms of mononuclear phagocyte accumulation in AD and discuss the potential roles of additional chemokines and their receptors in this process. We also propose a multi-step model for recruitment of mononuclear phagocytes into the brain. The first step involves egress of monocyte/microglial precursors from the bone marrow into the blood. The second step is crossing the blood-brain barrier to the perivascular areas and into the brain parenchyma. The final step includes movement of monocytes/microglia from areas of the brain that lack any amyloid deposition to senile plaques. Understanding the mechanism of recruitment of mononuclear phagocytes to the AD brain is necessary to further understand the role of these cells in the pathogenesis of AD and to identify any potential therapeutic use of these cells for the treatment of this disease.

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Authors: Hickman, S. E., & Khoury, J. E.
Affiliations: Harvard University (US)
ORCID: Hickman, Suzanne E.
Venue: CNS & Neurological Disorders - Drug Targets
Publisher: Bentham Science Publishers Ltd.
Published: 2010-04-01
Volume: 9
Issue: 2
Pages: 168-173
ISSN: 1568-007X (ISSN-L)
1871-5273
DOI: 10.2174/187152710791011982
PMC: PMC3684802
OpenAlex: W2060964242
Cited by: 120
References: 59
Citations by year: 2026: 8 · 2025: 4 · 2024: 8 · 2023: 4 · 2022: 1 · 2021: 5 · 2020: 9 · 2019: 6 · 2018: 8 · 2017: 11 · 2016: 11 · 2015: 8 · 2014: 12 · 2013: 9 · 2012: 7
FWCI: 4.85
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: CNS & Neurological Disorders - Drug Targets (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Neurological Disorders and Stroke (NS059005, R01NS059005)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: Alzheimer's disease, mononuclear phagocytes, monocytes, microglia, chemokines, MCP-1, CCR2, amyloid-beta, amyloid plaques, neuroinflammation, blood-brain barrier, monocyte recruitment
MeSH terms: Alzheimer Disease, Animals, Chemotaxis, Leukocyte, Encephalitis, Humans, Leukocytes, Mononuclear, Phagocytes, Amyloid beta-Peptides, Chemokine CCL2, Myeloid Progenitor Cells, Mice, Receptors, CCR2, Plaque, Amyloid

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Mechanisms of Mononuclear Phagocyte Recruitment in Alzheimers Disease

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