Evidence map›Paper›PMID 21902662›Full record

ArticleCurrent pharmaceutical design2011

Targeting mitochondrial bioenergetics for Alzheimer's prevention and treatment.

Jia Yao, Roberta Diaz Brinton

Abstract read
In one paragraph

Article in Current pharmaceutical design, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  5. Article
  6. Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025
    Review
  7. Creatine as a Therapeutic Target in Alzheimer's Disease.Current developments in nutrition · 2023
    Review
  8. Review
  9. Brain Metabolic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Allopregnanolone Reverses Bioenergetic Deficits in Female Triple Transgenic Alzheimer's Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Article
  15. Ketogenic Diet in Alzheimer's Disease.International journal of molecular sciences · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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 1 institution in 1 country.

Jia YaoDepartment of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, 90033, USA.
Roberta Diaz Brinton
University of Southern California · US

Funding

Estrogen-Induced Neuroprotective Mitochondrial MechanismR01AG032236 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BRINTON, ROBERTA EILEEN · 2009 to 2013
$1.6M
NIA NIH HHS 2R01AG032236NIA NIH HHS R01 AG032236
6 · The paper itself

Abstract

Alzheimer's is a neurodegenerative disease with a complex and progressive pathological phenotype characterized first by hypometabolism and impaired mitochondrial bioenergetics followed by pathological burden. The progressive and multifaceted degenerative phenotype of Alzheimer's suggests that successful treatment strategies necessarily will be equally multi-faceted and disease stage specific. Traditional therapeutic strategies based on the pathological aspect of the disease have achieved success in preclinical models which has not translated into clinical therapeutic efficacy. Meanwhile, increasing evidence indicates an antecedent and potentially causal role of mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress in AD pathogenesis. The essential role of mitochondrial bioenergetics and the unique trajectory of alterations in brain metabolic capacity enable a bioenergetic- centric strategy that targets disease-stage specific pattern of brain metabolism for disease prevention and treatment. A combination of nutraceutical and pharmaceutical intervention that enhances glucose-driven metabolic activity and potentiates mitochondrial bioenergetic function could prevent the antecedent decline in brain glucose metabolism, promote healthy aging and prevent AD. Alternatively, during the prodromal incipient phase of AD, sustained activation of ketogenic metabolic pathways coupled with supplement of the alternative fuel source, ketone bodies, could sustain mitochondrial bioenergetic function to prevent or delay further progression of the disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCentral Nervous System AgentsHumansMitochondriaMolecular Targeted TherapyOxidative StressAmyloid beta-PeptidesCentral Nervous System Agents

Identifiers

PMID21902662
PMCPMC4209948
OpenAlexW2120395583

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.