Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Attenuation Aβ1-42-induced neurotoxicity in neuronal cell by 660nm and 810nm LED light irradiation

Thammasart S., Namchaiw P., Pasuwat K., Tonsomboon K., Khantachawana A.

Laboratory Study on Neuroinflammation, published in PLoS One (2023) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
PLoS One (2023)
Reported sample size
—
Source database
Europe PMC
PMID
37478089
PMCID
PMC10361470
DOI
10.1371/journal.pone.0283976
Citations
12

Abstract (original English)

Oligomeric amyloid-β 1-42 (Aβ1-42) has a close correlation with neurodegenerative disorder especially Alzheimer's disease (AD). It induces oxidative stress and mitochondrial damage in neurons. Therefore, it is used to generate AD-like in vitro model for studying neurotoxicity and neuroprotection against amyloid-β. A low-level light therapy (LLLT) is a non-invasive method that has been used to treat several neurodegenerative disorders. In this study, the red wavelength (660nm) and near infrared wavelength (810nm) at energy densities of 1, 3, and 5 J/cm2 were used to modulate biochemical processes in the neural cells. The exposure of Aβ1-42 resulted in cell death, increased intracellular reactive oxygen species (ROS), and retracted neurite outgrowth. We showed that both of LLLT wavelengths could protect neurons form Aβ1-42-induced neurotoxicity in a biphasic manner. The treatment of LLLT at 3 J/cm2 potentially alleviated cell death and recovered neurite outgrowth. In addition, the treatment of LLLT following Aβ1-42 exposure could attenuate the intracellular ROS generation and Ca2+ influx. Interestingly, both wavelengths could induce minimal level of ROS generation. However, they did not affect cell viability. In addition, LLLT also stimulated Ca2+ influx, but not altered mitochondrial membrane potential. This finding indicated LLLT may protect neurons through the stimulation of s

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
NeuronsHumansAlzheimer DiseaseNeurotoxicity SyndromesCalciumReactive Oxygen SpeciesPeptide FragmentsApoptosisCell SurvivalAmyloid beta-Peptides

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