Monocyte Chemoattractant Protein‐1 Plays a Dominant Role in the Chronic Inflammation Observed in Alzheimer's Disease
Open accessAbstract
Chronic neuroinflammation correlates with cognitive decline and brain atrophy in Alzheimer's disease (AD), and cytokines and chemokines mediate the inflammatory response. However, quantitation of cytokines and chemokines in AD brain tissue has only been carried out for a small number of mediators with variable results. We simultaneously quantified 17 cytokines and chemokines in brain tissue extracts from controls (n = 10) and from patients with and without genetic forms of AD (n = 12). Group comparisons accounting for multiple testing revealed that monocyte chemoattractant protein‐1 (MCP‐1), interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8) were consistently upregulated in AD brain tissue. Immunohistochemistry for MCP‐1, IL‐6 and IL‐8 confirmed this increase and determined localization of these factors in neurons (MCP‐1, IL‐6, IL‐8), astrocytes (MCP‐1, IL‐6) and plaque pathology (MCP‐1, IL‐8). Logistic linear regression modeling determined that MCP‐1 was the most reliable predictor of disease. Our data support previous work on significant increases in IL‐6 and IL‐8 in AD but indicate that MCP‐1 may play a more dominant role in chronic inflammation in AD.
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CCL2 is implicated in the chronic neuroinflammation accompanying Alzheimer's disease, and its cerebrospinal fluid levels predict a faster rate of cognitive decline in AD.
“In particular, CCL2, a proinflammatory chemokine, is implicated in the chronic neuroinflammation accompanying AD,18 and its cerebrospinal fluid levels predict a faster rate of cognitive decline in AD.19”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [18]
CCL2 is a proinflammatory chemokine implicated in the chronic neuroinflammation accompanying AD.
“a proinflammatory chemokine implicated in the chronic neuroinflammation accompanying AD.18”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [18]
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- Authors
- Sokolova, A., Hill, M. D., Rahimi, F., Warden, L. A., Halliday, G. M., & Shepherd, C. E.
- Affiliations
- Neuroscience Research Australia (AU)
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2009-06-10
- Volume
- 19
- Issue
- 3
- Pages
- 392-398
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8094842
- OpenAlex
- W2091102323
- Cited by
- 249
- References
- 52
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 13 · 2023: 21 · 2022: 13 · 2021: 22 · 2020: 12 · 2019: 11 · 2018: 14 · 2017: 10 · 2016: 15 · 2015: 15 · 2014: 16 · 2013: 10 · 2012: 7
- FWCI
- 9.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, MCP-1, neuroinflammation, cytokines, chemokines, interleukin-6, interleukin-8, amyloid plaques, astrocytes, neurons, biomarkers, brain tissue
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Astrocytes, Brain, Female, Humans, Immunohistochemistry, Inflammation, Male, Middle Aged, Neurons, Interleukin-6, Interleukin-8, Chemokine CCL2, Plaque, Amyloid
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