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Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model
Kook SY, Jeong H, Kang MJ, Park R, Shin HJ, Han SH, Son SM, Song H et al.. Cell death and differentiation, 2014-05-23
Topic: Brain proteins, microglia and lab models
Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. Although marked reductions of CB expression have been observed in the brains of mice and humans with Alzheimer disease (AD), it is unknown whether these changes contribute to AD-related dysfunction. To determine the pathogenic importance of CB depletions in AD models, we crossed 5 familial AD mutations (5XFAD; Tg) mice with CB knock-out (CBKO) mice and generated a novel line CBKO·5XFAD (CBKOTg) mice.
Key findings
- Although marked reductions of CB expression have been observed in the brains of mice and humans with Alzheimer disease (AD), it is unknown whether these changes contribute to AD-related dysfunction.
- To determine the pathogenic importance of CB depletions in AD models, we crossed 5 familial AD mutations (5XFAD; Tg) mice with CB knock-out (CBKO) mice and generated a novel line CBKO·5XFAD (CBKOTg) mice.
- We first identified the change of signaling pathways and differentially expressed proteins globally by removing CB in Tg mice using mass spectrometry and antibody microarray.
- Immunohistochemistry showed that CBKOTg mice had significant neuronal loss in the subiculum area without changing the magnitude (number) of amyloid β-peptide (Aβ) plaques deposition and elicited significant apoptotic features and mitochondrial dysfunction compared with Tg mice.
Why it matters
Mice with familial Alzheimer's disease mutations were crossed with calbindin-D28k knockout mice to study the role of calbindin-D28k in disease-related dysfunction. This is an animal study and does not show any treatment, cure, or prevention for Alzheimer's disease in humans.
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Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cell death and differentiation) |
| Journal's citation record | 3 / 4 | Cell Death and Differentiation: journal h-index 313 (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 | 2014 — 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 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 111 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.9 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 3 / 6 | Cited 4.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 29 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Inhee Mook‐Jung: h-index 71 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24853300) |
| Free to read | 2 / 2 | Free to read |
| Total | 47 / 100 | — |
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Read the original
- DOI: 10.1038/cdd.2014.67
- PubMed: 24853300
- Original source →
- Free full text: Cell Death and Differentiation →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Kook, S. Y., Jeong, H., Kang, M. J., Park, R., Shin, H. J., Han, S. H., et al. (2014). Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model. Cell death and differentiation. https://doi.org/10.1038/cdd.2014.67
Vancouver
Kook SY, Jeong H, Kang MJ, Park R, Shin HJ, Han SH, et al. Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model. Cell death and differentiation. 2014. doi:10.1038/cdd.2014.67. PMID: 24853300.
BibTeX
@article{kook2014-24853300,
author = {Kook, S. Y. and Jeong, H. and Kang, M. J. and Park, R. and Shin, H. J. and Han, S. H. and Son, S. M. and Song, H. and others},
title = {{Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model}},
journal = {Cell death and differentiation},
year = {2014},
doi = {10.1038/cdd.2014.67},
pmid = {24853300},
url = {https://doi.org/10.1038/cdd.2014.67}
}
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