Evidence map›Paper›PMID 27662318›Full record

ReviewJournal of Alzheimer's disease : JAD2017

Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer's Disease.

Lan Guo, Jing Tian, Heng Du

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 5% 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

124 citing papers in PubMed, 3 syntheses or guidelines pooled it, 206 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  7. The Alzheimer's disease risk gene SORL1 is a regulator of excitatory neuronal function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. How deep is your recovery? Rethinking true motor recovery versus compensation in neurorehabilitation.International journal of rehabilitation research. Internationale Zeitschrift fur Rehabilitationsforschung. Revue internationale de recherches de readaptation · 2026
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. A blood based mitochondrial functional index biomarker for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  19. Article
  20. Article

64 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

3 authors at 2 institutions in 2 countries.

Lan GuoDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX, USA.
Jing TianDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX, USA.
Heng DuDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX, USA.
The University of Texas at Dallas · USShandong University · CN

Funding

Mitochondrial ATP Synthase Dysfunction and Synaptic Stress in Alzheimer's DiseaseR01AG053588 · NIA · UNIVERSITY OF TEXAS DALLAS · PI DU, HENG · 2016 to 2020
$1.9M
Mitochondrial pore and synaptic stress in Alzheimer's diseaseR00AG037716 · NIA · UNIVERSITY OF TEXAS DALLAS · PI DU, HENG · 2013 to 2015
$740k
NIA NIH HHS R00 AG037716NIA NIH HHS R01 AG053588
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disorder, in which multiple risk factors converge. Despite the complexity of the etiology of the disease, synaptic failure is the pathological basis of cognitive impairment, the cardinal sign of AD. Decreased synaptic density, compromised synaptic transmission, and defected synaptic plasticity are hallmark synaptic pathologies accompanying AD. However, the mechanisms by which synapses are injured in AD-related conditions have not been fully elucidated. Mitochondria are a critical organelle in neurons. The pivotal role of mitochondria in supporting synaptic function and the concomitant occurrence of mitochondrial dysfunction with synaptic stress in postmortem AD brains as well as AD animal models seem to lend the credibility to the hypothesis that mitochondrial defects underlie synaptic failure in AD. This concept is further strengthened by the protective effect of mitochondrial medicine on synaptic function against the toxicity of amyloid-β, a key player in the pathogenesis of AD. In this review, we focus on the association between mitochondrial dysfunction and synaptic transmission deficits in AD. Impaired mitochondrial energy production, deregulated mitochondrial calcium handling, excess mitochondrial reactive oxygen species generation and release play a crucial role in mediating synaptic transmission deregulation in AD. The understanding of the role of mitochondrial dysfunction in synaptic stress may lead to novel therapeutic strategies for the treatment of AD through the protection of synaptic transmission by targeting to mitochondrial deficits.

Indexed as

Alzheimer DiseaseAnimalsHumansMitochondriaMitochondrial DiseasesSynaptic TransmissionAlzheimer’s diseasemitochondrial dysfunctionsynaptic injurysynaptic mitochondriasynaptic transmission

Identifiers

PMID27662318
PMCPMC5605817
OpenAlexW2522744939

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.