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Related Experiment Video

Updated: Apr 18, 2026

Near Infrared NIr Light Increases Expression of a Marker of Mitochondrial Function in the Mouse Vestibular Sensory Epithelium
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Optimizing Brain Biology Through Near-Infrared-Induced Mitochondrial Melatonin Synthesis: A Hypothesis Paper.

Joseph Mercola1

  • 1Family Medicine, Midwestern University Chicago College of Osteopathic Medicine, Downers Grove, USA.

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|April 17, 2026
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Summary

Near-infrared (NIR) radiation may protect brain cells by activating mitochondrial melatonin synthesis, a process dependent on glutathione precursors. This pathway offers a potential neuroprotective mechanism against oxidative damage.

Keywords:
alzheimer's diseasecytochrome c oxidaseglutathionemitochondrial melatoninnear-infrared lightneuroprotectionphotobiomodulation

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Area of Science:

  • Neuroscience and mitochondrial biology
  • Investigating the role of light exposure and endogenous compounds in brain health

Background:

  • The brain's high energy demand makes neurons susceptible to oxidative stress.
  • Reduced exposure to near-infrared (NIR) radiation and age-related declines in melatonin and mitochondrial function are linked to neurodegeneration.
  • Glutathione precursor availability may limit antioxidant capacity during aging.

Purpose of the Study:

  • To propose a mechanistic framework for neuroprotection via NIR radiation-activated mitochondrial melatonin synthesis.
  • To integrate evidence from photobiomodulation, mitochondrial biology, and melatonin biochemistry.
  • To highlight the role of glutathione precursor availability as a critical factor.

Main Methods:

  • Targeted narrative synthesis of peer-reviewed literature (1990-2025).
  • Searches of PubMed, Web of Science, and Google Scholar using keywords like PBM, mitochondrial melatonin, glutathione, and neuroprotection.
  • Categorization of evidence strength to distinguish established findings from hypotheses.

Main Results:

  • Proposed a NIR-mitochondrial melatonin-glutathione cascade as a plausible neuroprotective mechanism.
  • Evidence supports individual components, but the integrated cascade requires experimental validation.
  • Glutathione precursor availability (glycine, cysteine) may be rate-limiting for this antioxidant cascade.

Conclusions:

  • NIR radiation may stimulate mitochondrial melatonin synthesis, initiating an antioxidant cascade for neuroprotection.
  • Adequate glutathione precursor substrate availability is crucial for this mechanism.
  • Further research is needed to validate this hypothesis, with potential implications for glycine and N-acetylcysteine (NAC) supplementation.