Evidence map›Paper›PMID 28059794›Full record

ReviewJournal of Alzheimer's disease : JAD2017

Oxidative Stress, Synaptic Dysfunction, and Alzheimer's Disease.

Eric Tönnies, Eugenia Trushina

Open access · bronzeAbstract readReview
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 828 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
828citing papers in PubMed, 1 pooled it
58.8field-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

828 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,692 citations in OpenAlex.

  1. Pooled it
  2. Article
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  7. Review
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  14. Intranasal Administration of Isoeugenol Improves Memory Deficits in APP/PS1 Old Mice-A Role Beyond Nrf2 Activation?FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  15. Review
  16. Article
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  20. Review

768 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.

Eric TönniesDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Eugenia TrushinaDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

Mitochondrial Complex I as a Target for Neuroprotection in ADRF1AG055549 · NIA · MAYO CLINIC ROCHESTER · PI TRUSHINA, EUGENIA · 2017 to 2025
$7.0M
Mitochondrial dynamics and metabolomic biomarkers in neurodegenerative disordersR01ES020715 · NIEHS · MAYO CLINIC ROCHESTER · PI TRUSHINA, EUGENIA · 2011 to 2015
$1.8M
NIA NIH HHS RF1 AG055549NIEHS NIH HHS R01 ES020715
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder without a cure. Most AD cases are sporadic where age represents the greatest risk factor. Lack of understanding of the disease mechanism hinders the development of efficacious therapeutic approaches. The loss of synapses in the affected brain regions correlates best with cognitive impairment in AD patients and has been considered as the early mechanism that precedes neuronal loss. Oxidative stress has been recognized as a contributing factor in aging and in the progression of multiple neurodegenerative diseases including AD. Increased production of reactive oxygen species (ROS) associated with age- and disease-dependent loss of mitochondrial function, altered metal homeostasis, and reduced antioxidant defense directly affect synaptic activity and neurotransmission in neurons leading to cognitive dysfunction. In addition, molecular targets affected by ROS include nuclear and mitochondrial DNA, lipids, proteins, calcium homeostasis, mitochondrial dynamics and function, cellular architecture, receptor trafficking and endocytosis, and energy homeostasis. Abnormal cellular metabolism in turn could affect the production and accumulation of amyloid-β (Aβ) and hyperphosphorylated Tau protein, which independently could exacerbate mitochondrial dysfunction and ROS production, thereby contributing to a vicious cycle. While mounting evidence implicates ROS in the AD etiology, clinical trials with antioxidant therapies have not produced consistent results. In this review, we will discuss the role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease.

Indexed as

Alzheimer DiseaseAnimalsHumansOxidative StressSynapsesAlzheimer’s diseaseamyloid-βantioxidantscaloric restrictionexercisemitochondriamitohormesisneurotransmissionoxidative stresssynaptic functiontau protein

Identifiers

PMID28059794
PMCPMC5409043
OpenAlexW2568450381

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.