Evidence map›Paper›PMID 22552779›Full record

ReviewMolecular neurobiology2012

Mitochondrial dysfunction--a pharmacological target in Alzheimer's disease.

Gunter P Eckert, Kathrin Renner, Schamim H Eckert, Janett Eckmann, Stephanie Hagl, Reham M Abdel-Kader, Christopher Kurz, Kristina Leuner, Walter E Muller

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Research in pharmaceutical sciences · 2024
    Article
  5. Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Effect of Ovocystatin on Amyloid β 1-42 Aggregation-In Vitro Studies.International journal of molecular sciences · 2023
    Article
  8. Mechanisms associated with the dysregulation of mitochondrial function due to lead exposure and possible implications on the development of Alzheimer's disease.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
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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

9 authors at 3 institutions in 2 countries.

Gunter P EckertDepartment of Pharmacology, Biocenter, Campus Riedberg, Goethe-University, Biocentre Geb. N260, R.1.09, Max-von-Laue Str. 9, 60438 Frankfurt, Germany. g.p.eckert@em.uni-frankfurt.de
Kathrin Renner
Schamim H Eckert
Janett Eckmann
Stephanie Hagl
Reham M Abdel-Kader
Christopher Kurz
Kristina Leuner
Walter E Muller
Goethe University Frankfurt · DEGerman University in Cairo · EGUniversity Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidences suggest that mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Alterations of mitochondrial efficiency and function are mainly related to alterations in mitochondrial content, amount of respiratory enzymes, or changes in enzyme activities leading to oxidative stress, mitochondrial permeability transition pore opening, and enhanced apoptosis. More recently, structural changes of the network are related to bioenergetic function, and its consequences are a matter of intensive research. Several mitochondria-targeting compounds with potential efficacy in AD including dimebon, methylene blue, piracetam, simvastatin, Ginkgo biloba, curcumin, and omega-3 polyunsaturated fatty acids have been identified. The majority of preclinical data indicate beneficial effects, whereas most controlled clinical trials did not meet the expectations. Since mitochondrial dysfunction represents an early event in disease progression, one reason for the disappointing clinical results could be that pharmacological interventions might came too late. Thus, more studies are needed that focus on therapeutic strategies starting before severe disease progress.

Indexed as

Alzheimer DiseaseAnimalsApoptosisBiological ProductsHumansMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOxidative StressBiological ProductsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore

Identifiers

PMID22552779
OpenAlexW2091746744

What OpenQuestion holds

Textmetadata
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.