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CCL2 Is Associated with a Faster Rate of Cognitive Decline during Early Stages of Alzheimer's Disease
Open accessAbstract
Chemokine (C-C motif) receptor 2 (CCR2)-signaling can mediate accumulation of microglia at sites affected by neuroinflammation. CCR2 and its main ligand CCL2 (MCP-1) might also be involved in the altered metabolism of beta-amyloid (Aβ) underlying Alzheimer's disease (AD). We therefore measured the levels of CCL2 and three other CCR2 ligands, i.e. CCL11 (eotaxin), CCL13 (MCP-4) and CCL26 (eotaxin-3), in the cerebrospinal fluid (CSF) and plasma of 30 controls and 119 patients with mild cognitive impairment (MCI) at baseline. During clinical follow-up 52 MCI patients were clinically stable for five years, 47 developed AD (i.e. cases with prodromal AD at baseline) and 20 developed other dementias. Only CSF CCL26 was statistically significantly elevated in patients with prodromal AD when compared to controls (p = 0.002). However, in patients with prodromal AD, the CCL2 levels in CSF at baseline correlated with a faster cognitive decline during follow-up (r(s) = 0.42, p = 0.004). Furthermore, prodromal AD patients in the highest tertile of CSF CCL2 exhibited a significantly faster cognitive decline (p<0.001) and developed AD dementia within a shorter time period (p<0.003) compared to those in the lowest tertile. Finally, in the entire MCI cohort, CSF CCL2 could be combined with CSF Tau, P-tau and Aβ42 to predict both future conversion to AD and the rate of cognitive decline. If these results are corroborated in future studies, CCL2 in CSF could be a candidate biomarker for prediction of future disease progression rate in prodromal AD. Moreover, CCR2-related signaling pathways might be new therapeutic targets for therapies aiming at slowing down the disease progression rate of AD.
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“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 [19]
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“Importantly, the increase of these markers seems to be correlated with the cognitive impairment occurring in AD (Solfrizzi et al., 2006; Westin et al., 2012).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Westin et al., 2012
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Metadata
- Authors
- Westin, K., Buchhave, P., Nielsen, H., Minthon, L., Janciauskiene, S., & Hansson, O.
- Affiliations
- Lund University (SE)
- Medizinische Hochschule Hannover (DE)
- Corresponding author
- Hansson, Oskar
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-01-30
- Volume
- 7
- Issue
- 1
- Pages
- e30525
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3268759
- OpenAlex
- W2135955660
- Cited by
- 277
- References
- 28
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 30 · 2023: 11 · 2022: 29 · 2021: 27 · 2020: 21 · 2019: 20 · 2018: 11 · 2017: 23 · 2016: 10 · 2015: 18 · 2014: 21 · 2013: 21 · 2012: 5
- FWCI
- 13.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Lund University Publications (Lund University) (submittedVersion, other-oa)
- Funders
- Skåne County Council's Research and Development Foundation
- Vetenskapsrådet
- Swedish Brain Power
- Socialstyrelsen
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- MCP-1, CCR2, Alzheimer's disease, mild cognitive impairment, cognitive decline, cerebrospinal fluid biomarkers, CCL26, eotaxin, CCL13, conversion to Alzheimer's disease, tau protein, phosphorylated tau, amyloid-beta 42, disease progression prediction, chemokine signaling, neuroinflammation
- MeSH terms
- Aged, Alzheimer Disease, Cognition Disorders, Demography, Female, Follow-Up Studies, Humans, Male, Cohort Studies, Biomarkers, Linear Models, Disease Progression, Chemokine CCL2, Cognitive Dysfunction
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