Evidence map›Paper›PMID 21470101›Full record

ReviewCurrent Alzheimer research2011

Mitochondria as a therapeutic target for aging and neurodegenerative diseases.

P H Reddy, T P Reddy

Abstract readReview
In one paragraph

Review in Current Alzheimer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Brain-Resident Immune Cells in Neurodevelopmental Disorders.Advances in experimental medicine and biology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Saponins fromPharmaceutical biology · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2022
    Review

58 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

2 authors at 2 institutions in 1 country.

P H ReddyNeurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, OR 97006, USA. reddyh@ohsu.edu
T P Reddy
Oregon Health & Science University · USOregon National Primate Research Center · US

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's DiseaseR01AG028072 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI REDDY, P. HEMACHANDRA · 2007 to 2011
$1.5M
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
Synapse function in a mouse model of Alzheimer's diseaseR03AG026051 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI FRERKING, MATTHEW E · 2007 to 2008
$137k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163NCRR NIH HHS RR00163NIA NIH HHS AG020872NIA NIH HHS AG025061NIA NIH HHS R01 AG028072NIA NIH HHS R03 AG026051
6 · The paper itself

Abstract

Mitochondria are cytoplasmic organelles responsible for life and death. Extensive evidence from animal models, postmortem brain studies of and clinical studies of aging and neurodegenerative diseases suggests that mitochondrial function is defective in aging and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Several lines of research suggest that mitochondrial abnormalities, including defects in oxidative phosphorylation, increased accumulation of mitochondrial DNA defects, impaired calcium influx, accumulation of mutant proteins in mitochondria, and mitochondrial membrane potential dissipation are important cellular changes in both early and late-onset neurodegenerative diseases. Further, emerging evidence suggests that structural changes in mitochondria, including increased mitochondrial fragmentation and decreased mitochondrial fusion, are critical factors associated with mitochondrial dysfunction and cell death in aging and neurodegenerative diseases. This paper discusses research that elucidates features of mitochondria that are associated with cellular dysfunction in aging and neurodegenerative diseases and discusses mitochondrial structural and functional changes, and abnormal mitochondrial dynamics in neurodegenerative diseases. It also outlines mitochondria-targeted therapeutics in neurodegenerative diseases.

Indexed as

AgingAnimalsBrainDNA, MitochondrialHumansMitochondriaMitochondrial DiseasesModels, BiologicalNeurodegenerative DiseasesDNA, Mitochondrial

Identifiers

PMID21470101
PMCPMC3295247
OpenAlexW2082841638

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.