Evidence map›Paper›PMID 19362755›Full record

ArticleNeurobiology of aging2011

Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model.

Heng Du, Lan Guo, Wensheng Zhang, Monika Rydzewska, Shidu Yan

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

147 citing papers in PubMed, 223 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Mitochondrial CaBiomolecules · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

87 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 2 countries.

Heng DuDepartment of Surgery, and Taub Institute for Research on Alzheimer's Disease and Aging Brain, College of Physicians & Surgeons of Columbia University, 650 West 168th Street, New York, NY 10032, USA.
Lan Guo
Wensheng Zhang
Monika Rydzewska
Shidu Yan
Columbia University · US

Funding

Satellite Diagnostic and Treatment Clinic CoreP50AG008702 · NIA · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI DE JAGER, PHILIP L · 1989 to 2019
$46.3M
STRUCTURAL AND FUNCTIONAL PROPERTIESP01AG017490 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2000 to 2010
$16.9M
NIA NIH HHS P01 AG017490NIA NIH HHS P01AG17490NIA NIH HHS P050 AG08702NIA NIH HHS P50 AG008702
6 · The paper itself

Abstract

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. 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). Cyp D deficient mAPP mice demonstrate less calcium-induced mitochondrial swelling, increased mitochondrial calcium uptake capacity, preserved mitochondrial respiratory function and improved spatial learning/memory even in old age (known to be the age for late stage AD pathology and synaptic dysfunction). These data demonstrate that abrogation of CypD results in persistent life-long protection against Aβ toxicity in an Alzheimer's disease mouse model, thereby suggesting that blockade of CypD may be of benefit for Alzheimer disease treatment.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsBrainCalciumCyclophilinsDisease Models, AnimalElectron Transport Complex IVHumansLearning DisabilitiesMaze LearningMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorCalciumCyclophilinsElectron Transport Complex IVMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FPPIF protein, mouse

Identifiers

PMID19362755
PMCPMC3304024
OpenAlexW1989331957

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.