April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
670nm LED Photobiomodulation is Retinoprotective in a Transgenic Mouse Model of Parkinson’s Disease
Author Affiliations & Notes
  • Michele Salzman
    Marshfield Clinic Research Foundation, Marshfield, WI
  • Kristina DeSmet
    Stiefel, a GSK Company, Raleigh-Durham, NC
  • Harry T Whelan
    Neurology, Medical College of Wisconsin, Milwaukee, WI
  • Ellen V Buchmann
    Neurology, Medical College of Wisconsin, Milwaukee, WI
  • Janis T Eells
    College of Health Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI
  • Footnotes
    Commercial Relationships Michele Salzman, None; Kristina DeSmet, None; Harry Whelan, None; Ellen Buchmann, None; Janis Eells, QBMI Photomedicine (C)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1913. doi:
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      Michele Salzman, Kristina DeSmet, Harry T Whelan, Ellen V Buchmann, Janis T Eells; 670nm LED Photobiomodulation is Retinoprotective in a Transgenic Mouse Model of Parkinson’s Disease. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1913.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by specific altered motor symptoms. These movement alterations are due to the loss of dopaminergic neurons in the substantia nigra and the accumulation of Lewy bodies consisting primarily of alpha-synuclein. Non-motor symptoms, including altered visual functions, are also associated with PD. Our laboratory previously documented the neuroprotective effects of 670nm LED photobiomodulation (PBM) in a transgenic mouse model of Parkinson’s disease. The purpose of the present study was to examine the potential of 670nm LED PBM to protect dopaminergic amacrine cells in the retina of these same mice.

Methods: Studies were conducted in a transgenic mouse model of PD that expresses the A53T mutation of alpha-synuclein. These transgenic mice develop a Parkinson’s-like syndrome characterized by neurodegenerative changes in the basal ganglia and severe motor dysfunction. Two therapeutic protocols were tested, a prevention protocol and a treatment protocol. For the prevention protocol, mice received 670nm LED PBM (300 sec at 25 mW/cm2; 7.5 J/cm2) or sham treatment 3 times weekly beginning at 2 months of age and extending to 20 months of age. For the treatment protocol, the 670nm LED PBM treatment was initiated at 8 months of age and extended to 20 months of age.

Results: The onset of Parkinsonian motor symptoms was significantly delayed in both therapeutic protocols. Moreover, striatal dopamine concentrations were significantly greater in the PBM-treated mice compared to sham-treated mice indicative of protection of the nigrostriatal pathway. Retinal dopamine concentrations were also significantly greater in PBM-treated mice than in sham-treated mice indicative of protection of dopaminergic amacrine cells in the retina.

Conclusions: These data document the neuroprotective and retinoprotective actions of 670nm LED PBM in an experimental model of PD and support the potential of PBM in the treatment of Parkinson’s disease.

Keywords: 688 retina • 615 neuroprotection • 416 amacrine cells  
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