Therapeutic effect of near infrared (NIR) light on Parkinson's disease models.

Parkinson's disease (PD) is a neurodegenerative disorder that affects large numbers of people, particularly those of a more advanced age. Mitochondrial dysfunction plays a central role in PD, especially in the electron transport chain. This mitochondrial role allows the use of inhibitors of complex I and IV in PD models, and enhancers of complex IV activity, such as NIR light, to be used as possible therapy. PD models fall into two main categories; cell cultures and animal models. In cell cultures, primary neurons, mutant neuroblastoma cells, and cell cybrids have been studied in conjunction with NIR light. Primary neurons show protection or recovery of function and morphology by NIR light after toxic insult. Neuroblastoma cells, with a gene for mutant alpha-synuclein, show similar results. Cell cybrids, containing mtDNA from PD patients, show restoration of mitochondrial transport and complex I and IV assembly. Animal models include toxin-insulted mice, and alpha-synuclein transgenic mice. Functional recovery of the animals, chemical and histological evidence, and delayed disease progression show the potential of NIR light in treating Parkinson's disease.

[1]  E. Junn,et al.  Human α-Synuclein over-expression increases intracellular reactive oxygen species levels and susceptibility to dopamine , 2002, Neuroscience Letters.

[2]  H. T. Whelan,et al.  Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity , 2008, Neuroscience.

[3]  J. Bennett,et al.  The cybrid model of sporadic Parkinson's disease , 2009, Experimental Neurology.

[4]  M. Wong-Riley,et al.  Photobiomodulation partially rescues visual cortical neurons from cyanide-induced apoptosis , 2006, Neuroscience.

[5]  Keyoumars Ashkan,et al.  Neuroprotection of midbrain dopaminergic cells in MPTP‐treated mice after near‐infrared light treatment , 2010, The Journal of comparative neurology.

[6]  C. C. Johnson,et al.  The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living , 1998, Neurology.

[7]  Todd B. Sherer,et al.  Chronic systemic pesticide exposure reproduces features of Parkinson's disease , 2000, Nature Neuroscience.

[8]  Noel T. Whelan,et al.  NASA light-emitting diodes for the prevention of oral mucositis in pediatric bone marrow transplant patients. , 2002, Journal of clinical laser medicine & surgery.

[9]  M. Beal,et al.  Parkinson's disease. , 2007, Human molecular genetics.

[10]  M. Wong-Riley,et al.  Light-emitting diode treatment reverses the effect of TTX on cytochrome oxidase in neurons , 2001, Neuroreport.

[11]  Andrew B West,et al.  Molecular pathophysiology of Parkinson's disease. , 2005, Annual review of neuroscience.

[12]  P. Praamstra,et al.  Genetic and environmental risk factors in Parkinson’s disease , 1998, Clinical Neurology and Neurosurgery.

[13]  T. Sherer,et al.  Environment, Mitochondria, and Parkinson's Disease , 2002, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry.

[14]  R. Gainetdinov,et al.  Role of Dopamine Transporter in Methamphetamine-Induced Neurotoxicity: Evidence from Mice Lacking the Transporter , 1998, The Journal of Neuroscience.

[15]  Britton Chance,et al.  Photobiomodulation Directly Benefits Primary Neurons Functionally Inactivated by Toxins , 2005, Journal of Biological Chemistry.

[16]  L. Tremblay,et al.  Experimental Models of Parkinson’s Disease , 2002, Annales pharmaceutiques francaises.

[17]  W. Dauer,et al.  Parkinson's Disease Mechanisms and Models , 2003, Neuron.

[18]  Noel T. Whelan,et al.  Therapeutic photobiomodulation for methanol-induced retinal toxicity , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[19]  T. Dawson,et al.  Oxidative Stress and Genetics in the Pathogenesis of Parkinson's Disease , 2000, Neurobiology of Disease.

[20]  Noel T. Whelan,et al.  Effect of NASA light-emitting diode irradiation on wound healing. , 2001, Journal of clinical laser medicine & surgery.

[21]  Rong Ying,et al.  Pretreatment with near-infrared light via light-emitting diode provides added benefit against rotenone- and MPP+-induced neurotoxicity , 2008, Brain Research.

[22]  N. Wood,et al.  Molecular pathogenesis of Parkinson's disease. , 2005, Human molecular genetics.

[23]  T. Karu,et al.  Primary and secondary mechanisms of action of visible to near-IR radiation on cells. , 1999, Journal of photochemistry and photobiology. B, Biology.

[24]  Rina Das,et al.  Effect of NASA light-emitting diode irradiation on molecular changes for wound healing in diabetic mice. , 2003, Journal of clinical laser medicine & surgery.

[25]  Y. Yang,et al.  Enhanced vulnerability to oxidative stress by alpha-synuclein mutations and C-terminal truncation. , 2000, Neuroscience.

[26]  M. Beal,et al.  Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases , 2006, Nature.

[27]  U. Oron,et al.  Reduced axonal transport in Parkinson's disease cybrid neurites is restored by light therapy , 2009, Molecular Neurodegeneration.

[28]  M. Chesselet,et al.  Genetic mouse models of parkinsonism: Strengths and limitations , 2005, NeuroRX.

[29]  R. Gainetdinov,et al.  Dopamine Transporter Is Required for In Vivo MPTP Neurotoxicity: Evidence from Mice Lacking the Transporter , 1997, Journal of neurochemistry.

[30]  M. Wong-Riley,et al.  Harnessing the cell's own ability to repair and prevent neurodegenerative disease. , 2008, SPIE newsroom.