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CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer's disease
Westin K, Buchhave P, Nielsen H, Minthon L, Janciauskiene S, Hansson O.. PloS one, 2012-01-30
Topic: Amyloid, tau and blood-test diagnosis
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.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Westin, K., Buchhave, P., Nielsen, H., Minthon, L., Janciauskiene, S., & Hansson, O. (2012). CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer's disease. PloS one. https://doi.org/10.1371/journal.pone.0030525
Vancouver
Westin K, Buchhave P, Nielsen H, Minthon L, Janciauskiene S, Hansson O. CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer's disease. PloS one. 2012. doi:10.1371/journal.pone.0030525. PMID: 22303443.
BibTeX
@article{westin2012-22303443,
author = {Westin, K. and Buchhave, P. and Nielsen, H. and Minthon, L. and Janciauskiene, S. and Hansson, O.},
title = {{CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer's disease}},
journal = {PloS one},
year = {2012},
doi = {10.1371/journal.pone.0030525},
pmid = {22303443},
url = {https://doi.org/10.1371/journal.pone.0030525}
}
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Key findings
- Only CSF CCL26 was statistically significantly elevated in patients with prodromal AD when compared to controls (p = 0.002).
- 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.
- 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.
Why it matters
Among 119 people with mild cognitive impairment, those who went on to develop Alzheimer's disease and had higher levels of CCL2 in cerebrospinal fluid declined faster and developed dementia sooner. The authors state that CCL2 could be a candidate biomarker for predicting disease progression if these results are confirmed in future studies.
Study details
- Participants119
- Evidence strengthModerate
How this study scored 58/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (PloS one) |
| Journal's citation record | 4 / 4 | PLoS ONE: journal h-index 594 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 2 / 4 | 119 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 279 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 17.4 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 4 / 6 | Cited 12.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 16 other studies in this library |
| Still being cited | 3 / 4 | Cited 61 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Oskar Hansson: h-index 148 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Lund University: institution h-index 1,119 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22303443) |
| Free to read | 2 / 2 | Free to read |
| Total | 58 / 100 | — |
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