Evidence map›Paper›PMID 29118388›Full record

ArticleScientific reports2017

Near infrared light decreases synaptic vulnerability to amyloid beta oligomers.

Michele M Comerota, Balaji Krishnan, Giulio Taglialatela

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Transcranial near-infrared therapy restores synaptic resilience by reshaping signaling landscapes in sleep-deprived tauopathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Review
  4. Article
  5. Hippocampal Neural Stem Cell Exosomes Promote Brain Resilience against the Impact of Tau Oligomers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  6. Article
  7. Article
  8. Photobiomodulation for Neurodegenerative Diseases: A Scoping Review.International journal of molecular sciences · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Photobiomodulation for Hypertension and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022
    Review
  20. Article
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 1 institution in 1 country.

Michele M ComerotaMitchell Center for Neurodegenerative Diseases, Department of Neurology, University of Texas Medical Branch, Galveston, TX, USA. mmcomero@utmb.edu.
Balaji KrishnanMitchell Center for Neurodegenerative Diseases, Department of Neurology, University of Texas Medical Branch, Galveston, TX, USA. bakrishn@utmb.edu.ORCID 0000-0003-2074-4165
Giulio TaglialatelaMitchell Center for Neurodegenerative Diseases, Department of Neurology, University of Texas Medical Branch, Galveston, TX, USA. gtaglial@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

Mechanisms of resistance to cognitive decline in ADR01AG042890 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI TAGLIALATELA, GIULIO · 2013 to 2017
$1.5M
6 · The paper itself

Abstract

Synaptic dysfunction due to the disrupting binding of amyloid beta (Aβ) and tau oligomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation. Consequently, there is ample consensus that preventing early synaptic dysfunction would be an effective therapeutic strategy for AD. With this goal in mind, we investigated the effect of a treatment of mice with near infrared (NIR) light on synaptic vulnerability to Aβ oligomers. We found that Aβ oligomer binding to CNS synaptosomes isolated from wild type (wt) mice treated with NIR light was significantly reduced and the resulting suppression of long term potentiation (LTP) by Aβ oligomers was prevented. Similarly, APP transgenic mice treated with NIR showed a significant reduction of endogenous Aβ at CNS synapses. We further found that these phenomena were accompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 mice. This study provides evidence that NIR light can effectively reduce synaptic vulnerability to damaging Aβ oligomers, thus furthering NIR light therapy as a viable treatment for AD.

Indexed as

Infrared RaysAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleHumansLong-Term PotentiationMaleMembrane Potential, MitochondrialMice, Inbred C57BLMice, TransgenicProtein BindingSynapsesSynaptosomesAmyloid beta-PeptidesAmyloid beta-Protein Precursor

Identifiers

PMID29118388
PMCPMC5678170
OpenAlexW2766163058

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.