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Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model
Du H, Guo L, Zhang W, Rydzewska M, Yan S.. Neurobiology of aging, 2009-04-11
Topic: Brain proteins, microglia and lab models
Mitochondrial stress is one of the early features of Alzheimer disease (AD). Mitochondrial Aβ has been linked to mitochondrial toxicity. Our recent study demonstrated that cyclophilin D (CypD) mediated mitochondrial permeability transition pore (mPTP) is an important mechanism for neuronal and synaptic stress induced by both Aβ and oxidative stress.
Key findings
- Mitochondrial Aβ has been linked to mitochondrial toxicity.
- Our recent study demonstrated that cyclophilin D (CypD) mediated mitochondrial permeability transition pore (mPTP) is an important mechanism for neuronal and synaptic stress induced by both Aβ and oxidative stress.
- In transgenic AD-type mice overexpressing mutant amyloid precursor protein (APP) and Aβ (mAPP), CypD deficiency improves mitochondrial and synaptic function and learning/memory up to 12 months old.
- Here we provide evidence of the protective effects of CypD deficiency in aged AD mice (22-24 months).
Why it matters
In transgenic mice overexpressing mutant APP and amyloid beta, cyclophilin D deficiency improved mitochondrial and synaptic function and learning and memory up to 12 months old. This is an animal study and does not show that the same approach helps people.
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Study details
- Evidence strengthLow
How this study scored 36/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 23 of the 64 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2011 — 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 | — / 7 | No citation count (OpenAlex dates this DOI to 2009, the record says 2011; OpenAlex values not used) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19362755) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 23 / 64 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 23 of the 64 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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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. Check the citation against the original before you use it.
APA 7th
Du, H., Guo, L., Zhang, W., Rydzewska, M., & Yan, S. (2011). Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2009.03.003
Vancouver
Du H, Guo L, Zhang W, Rydzewska M, Yan S. Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model. Neurobiology of aging. 2011. doi:10.1016/j.neurobiolaging.2009.03.003. PMID: 19362755.
BibTeX
@article{du2011-19362755,
author = {Du, H. and Guo, L. and Zhang, W. and Rydzewska, M. and Yan, S.},
title = {{Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model}},
journal = {Neurobiology of aging},
year = {2011},
doi = {10.1016/j.neurobiolaging.2009.03.003},
pmid = {19362755},
url = {https://doi.org/10.1016/j.neurobiolaging.2009.03.003}
}
Later studies that cite this one
3 studies in the alzhub library list this one in their references.