Abstract
Neurons are metabolically protected against degeneration using low-level methylene blue and near-infrared light interventions. Both of these novel interventions act by a cellular mechanism involving enhancement of the electron transport chain in mitochondria, which promotes energy metabolism and neuronal survival (Gonzalez-Lima et al., 2014). Methylene blue preferentially enters neuronal mitochondria after systemic administration, and at low-doses forms an electron cycling redox complex that donates electrons to the mitochondrial electron transport chain. Low-level near-infrared light applied transcranially delivers photons to cortical neurons that are accepted by cytochrome oxidase, which causes increased cell respiration and cerebral blood flow. Breakthrough in vivo studies with these interventions suggest that targeting mitochondrial respiration may be beneficial for protection against different types of neurodegenerative disorders. The purpose of this paper is to provide an update on the cellular mechanisms mediating the neuroprotective effects of low doses of methylene blue and near-infrared light, and to argue that the neurotherapeutic benefits of these two different interventions share the same cellular mechanism of action based on stimulation of mitochondrial respiration. Presented first is the explanation of the biochemical redox action of low-dose methylene as an electron cycler on the mitochondrial electron transport. Presented second is the explanation of the biophysical action of near-infrared light as a photon donor to cytochrome oxidase that also serves to stimulate mitochondrial electron transport. We finish with a comparison of these two interventions and how they share a common cellular mechanism with similar properties such as energy transfer, low-dose hormetic dose-responses, and enhanced capacity for oxidative metabolic energy production, which serve to protect nervous tissue from degeneration.
Highlights
Neurons are metabolically protected against degeneration using low-level methylene blue and nearinfrared light interventions
The purpose of this paper is to provide an update on the cellular mechanisms mediating the neuroprotective effects of low doses of methylene blue and near-infrared light, and to argue that the neurotherapeutic benefits of these two different interventions share the same cellular mechanism of action based on stimulation of mitochondrial respiration
Near-infrared light from low-power lasers and light-emitting diodes (LEDs) stimulates mitochondrial respiration by donating photons that are absorbed by cytochrome oxidase, a bioenergetics process called photoneuromodulation in nervous tissue (Rojas and Gonzalez-Lima, 2013)
Summary
Low-dose methylene blue stimulates mitochondrial respiration by donating electrons to the electron transport chain. Because increased oxygen consumption by nerve cells is coupled to oxidative phosphorylation, ATP production increases as a consequence of the metabolic action of near-infrared light This type of luminous energy can enter brain mitochondria transcranially, and—independently of the electrons derived from food substrates—it can directly photostimulate cytochrome oxidase activity. Behavioral effects in humans can still be observed at 2 and 4 weeks after a single transcranial near-infrared light treatment (Barrett and Gonzalez-Lima, 2013) This enzymatic induction provides a long-tern mechanism for increasing the oxidative metabolic capacity of neurons, which is manifested in vivo by increases in cerebral rates of oxygen consumption and blood flow to the brain (Uozumi et al, 2010; Rojas et al, 2012b)
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