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Near-infrared (NIR) light passes readily through thescalp and skull and a small percentage of incident powerdensity can arrive at the cortical surface in humans.1 Theprimary photoreceptors for red and NIR light are mitochondria,and cortical neurons are exceptionally rich in mitochondria.It is likely that brain cells are ideally set up torespond to light therapy. The basic biochemical pathwaysactivated by NIR light, e.g., increased adenosine-5’-triphosphate(ATP) production, and signaling pathways activated byreactive oxygen species, nitric oxide release, and increasedcyclic adenosine monophosphate (AMP) all work together toproduce beneficial effects in brains whose function has beencompromised by ischemia, traumatic injury, or neurodegeneration.One of the main mechanisms of action of transcraniallight therapy (TLT) is to prevent neurons from dying, whenthey have been subjected to some sort of hypoxic, traumatic,or toxic insult. This is probably because of light-mediatedupregulation of cytoprotective gene products such as antioxidantenzymes, heat shock proteins, and anti-apoptoticproteins. Light therapy in vitro has been shown to protectneurons from death caused by methanol,2 cyanide or tetrodotoxin,3 and amyloid beta peptide.4There is also probably a second mechanism operating inTLT; increased neurogenesis. Neurogenesis is the generationof neuronal precursors and birth of new neural cells.5 Twokey sites for adult neurogenesis include the subventricularzone (SVZ) of the lateral ventricles, and the subgranularlayer (SGL) of the dentate gyrus in the hippocampus.6Neurogenesis can be stimulated by physiological factors,such as growth factors and environmental enrichment,and by pathological processes, including ischemia andneurodegeneration.7 Adult neurogenesis (in the hippocampusparticularly) is now recognized as a major determinantof brain function both in experimental animals and in humans.Neural progenitor cells in their niche in the SGL of thedentate gyrus give birth to newly formed neurons thatare thought to play a role in brain function, particularly inolfaction and in hippocampal-dependent learning and memory.  In small animal models neurogenesis can bereadily detected by incorporation of bromodeoxyuridine(BrdU), injected before euthanasia, into proliferating braincells. Increased neurogenesis after TLT, has been demonstratedin a rat model of stroke,9 and in the Hamblin laboratoryafter TLT for acute traumatic brain injury (TBI) in mice(W. Xuan, T. Ando, et al., unpublished data). These twomechanisms of action of TLT in ameliorating brain damage(prevention of neuronal death and increased neurogenesis)have motivated studies in both animals and humans for diversebrain disorders and diseases. TLT for acute stroke is themost developed,10 but acute TBI has also been shown tobenefit from TLT.11 These areas are reviewed further.United States. Dept. of Veterans Affairs. Medical Research ServiceNational Institutes of Health (U.S.) (Grant R01AI50875)Center for Integration of Medicine and Innovative Technology (DAMD17-02-2-0006)United States. Dept. of Defense. Congressionally Directed Medical Research Programs ( Program in TBI W81XWH-09-1-0514)United States. Air Force Office of Scientific Research (F9950-04-1-0079

Potential for Transcranial Laser or LED Therapy to Treat Stroke, Traumatic Brain Injury, and Neurodegenerative Disease