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CCR5 deficiency induces astrocyte activation, Abeta deposit and impaired memory function
Lee YK, Kwak DH, Oh KW, Nam SY, Lee BJ, Yun YW, Kim YB, Han SB et al.. Neurobiology of learning and memory, 2009-04-24
Topic: Brain proteins, microglia and lab models
Plain-language summary
Activation of astrocytes has been known to be associated with amyloid-beta (Abeta) deposit and production of pro-inflammatory cytokines and chemokines that lead to neuronal cell death in the pathogenesis of Alzheimer disease (AD). In the present study, we investigated whether the absence of CC chemokine receptor 5 (CCR5) results in activation of astrocytes, Abeta deposit and memory dysfunction in CCR5 knock (CCR5(-/-)) out mice. We found that long-term and spatial memory functions were impaired in CCR5(-/-) mice. There was a significant increased expression of glial fibrillary acidic protein (GFAP) in the brain of CCR5(-/-) mice as compared with that of wild type of CCR5 (CCR5(+/+)) mice. The expression of CCR5 was observed in CCR5(+/+) astrocytes, but was reduced in the CCR5(-/-) astrocytes even though the expression of GFAP was much higher. Paralleling with the activation of astorcytes, the Abeta(1-42) level was higher in the brains of CCR5(-/-) mice than that of CCR5(+/+) mice. Expression of beta-secretase (BACE1) and its product C99 was significantly elevated in CCR5(-/-) mice. The activation of CC chemokine receptor 2 (CCR2) causes activation of astrocytes that leads to Abeta deposit and memory dysfunction in CCR5(-/-) mice. In CCR5(-/-) mice, CCR2 expression was high and co-localized with GFAP. These findings suggest that the absence of CCR5 increases expression of CCR2, which leads to the activation of astrocytes causing Abeta deposit, and thereby impairs memory function. These results suggest that CCR5 may be a critical suppressor of the development and progression of AD pathology.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Lee, Y. K., Kwak, D. H., Oh, K. W., Nam, S. Y., Lee, B. J., Yun, Y. W., et al. (2009). CCR5 deficiency induces astrocyte activation, Abeta deposit and impaired memory function. Neurobiology of learning and memory. https://doi.org/10.1016/j.nlm.2009.04.003
Vancouver
Lee YK, Kwak DH, Oh KW, Nam SY, Lee BJ, Yun YW, et al. CCR5 deficiency induces astrocyte activation, Abeta deposit and impaired memory function. Neurobiology of learning and memory. 2009. doi:10.1016/j.nlm.2009.04.003. PMID: 19394434.
BibTeX
@article{lee2009-19394434,
author = {Lee, Y. K. and Kwak, D. H. and Oh, K. W. and Nam, S. Y. and Lee, B. J. and Yun, Y. W. and Kim, Y. B. and Han, S. B. and others},
title = {{CCR5 deficiency induces astrocyte activation, Abeta deposit and impaired memory function}},
journal = {Neurobiology of learning and memory},
year = {2009},
doi = {10.1016/j.nlm.2009.04.003},
pmid = {19394434},
url = {https://doi.org/10.1016/j.nlm.2009.04.003}
}
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Key findings
- Activation of astrocytes has been known to be associated with amyloid-beta (Abeta) deposit and production of pro-inflammatory cytokines and chemokines that lead to neuronal cell death in the pathogenesis of Alzheimer disease (AD).
- In the present study, we investigated whether the absence of CC chemokine receptor 5 (CCR5) results in activation of astrocytes, Abeta deposit and memory dysfunction in CCR5 knock (CCR5(-/-)) out mice.
- We found that long-term and spatial memory functions were impaired in CCR5(-/-) mice.
- There was a significant increased expression of glial fibrillary acidic protein (GFAP) in the brain of CCR5(-/-) mice as compared with that of wild type of CCR5 (CCR5(+/+)) mice.
- Expression of beta-secretase (BACE1) and its product C99 was significantly elevated in CCR5(-/-) mice.
Why it matters
CCR5 knockout mice showed impaired long-term and spatial memory, increased GFAP, higher Abeta(1-42) levels and elevated BACE1 and C99. These are mouse findings about CCR5 absence and Alzheimer-like changes, not a treatment or prevention result in humans.
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Study details
- Evidence strengthLow
How this study scored 37/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of learning and memory) |
| Journal's citation record | 2 / 4 | Neurobiology of Learning and Memory: journal h-index 155 (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 | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2009 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 58 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.1 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 2 / 6 | Cited 1.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 1 / 4 | Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Jin Tae Hong: h-index 74 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Chungbuk National University: institution h-index 323 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19394434) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
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