The impact of near-infrared light on dopaminergic cell survival in a transgenic mouse model of parkinsonism

Purushothuman, Sivaraman; Nandasena, Charith; Johnstone, Daniel M.; Stone, Jonathan; Mitrofanis, John

doi:10.1016/j.brainres.2013.08.047

Cited by 64 publications

(53 citation statements)

References 38 publications

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“…If cells lose TH expression, then they are likely to undergo death subsequently [34][35][36], which then leads to a reduction in Nissl-stained (and TH + ) cell number [31,32]. Notwithstanding a small number of cells that may have transient loss of TH expression, a key aspect of our study was whether NIr treatment saved TH expression during a period when MPTP treatment alone would have abolished it [15][16][17][18][19][20]. Fig 2 shows the estimated number of TH + cells in the SNc of the different groups in the 2d (Fig 2A), 7d ( Fig 2B) and 14d (Fig 2C) series.…”

Section: Substantia Nigra Pars Compacta (Snc)mentioning

confidence: 99%

“…There have also been several in vivo explorations in animal models of the disease. For example, as assessed by expression of the marker tyrosine hydroxylase (TH), NIr treatment has been shown to mitigate loss of TH + cells in the well-known MPTP (1-methyl-4phenyl-1,2,3,6-tetrahydropyridine) mouse model [15][16][17][18][19], as well as in a transgenic mouse model (K369I) of Parkinson's disease [20].…”

Section: The Effect Of Different Doses Of Near Infrared Light On Dopamentioning

confidence: 99%

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The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

Massri

Johnstone

Peoples

et al. 2015

International Journal of Neuroscience

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We have used the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model to explore whether (i) the neuroprotective effect of near infrared light (NIr) treatment in the SNc is dose-dependent and (ii) the relationship between tyrosine hydroxylase (TH)+ terminal density and glial cells in the caudate-putamen complex (CPu). Mice received MPTP injections (50 mg/kg) and 2 J/cm2 NIr dose with either 2 d or 7 d survival period. In another series, with a longer 14 d survival period, mice had a stronger MPTP regime (100 mg/kg) and either 2 J/cm2 or 4 J/cm2 NIr dose. Brains were processed for routine immunohistochemistry and cell counts were made using stereology. Our findings were that in the 2 d series, no change in SNc TH+ cell number was evident after any treatment. In the 7 d series however, MPTP insult resulted in ∼45% reduction in TH+ cell number; after NIr (2 J/cm2) treatment, many cells were protected from the toxic insult. In the 14 d series, MPTP induced a similar reduction in TH+ cell number. NIr mitigated the loss of TH+ cells, but only at the higher dose of 4 J/cm2; the lower dose of 2 J/cm2 had no neuroprotective effect in this series. The higher dose of NIr, unlike the lower dose, also mitigated the MPTP- induced increase in CPu astrocytes after 14 d; these changes were independent of TH+ terminal density, of which, did not vary across the different experimental groups. In summary, we showed that neuroprotection by NIr irradiation in MPTP-treated mice was dose-dependent; with increasing MPTP toxicity, higher doses of NIr were required to protect cells and reduce astrogliosis.

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Section: Substantia Nigra Pars Compacta (Snc)mentioning

confidence: 99%

Section: The Effect Of Different Doses Of Near Infrared Light On Dopamentioning

confidence: 99%

The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

Massri

Johnstone

Peoples

et al. 2015

International Journal of Neuroscience

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“…45,51 In cultures of human neuroblastoma cells engineered to overexpress alpha-synuclein, light therapy has been reported to increase mitochondrial function and reduce oxidative stress after MPP + exposure. 79,80 Further, mitochondrial movement along axons in hybrid cells bearing mitochondrial DNA from Parkinson's disease patients improves substantially after light therapy (810 nm, laser), with movement restored to near control levels. 81 The view from the animal model: the in vivo evidence…”

Section: Basic Science and Clinical Evidence For Neuroprotection By Lmentioning

confidence: 96%

The potential of light therapy in Parkinson's disease

Johnstone¹,

Coleman²,

Moro³

et al. 2014

CPT

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Parkinson's disease is a movement disorder with cardinal signs of resting tremor, akinesia, and rigidity. These manifest after a progressive death of many dopaminergic neurons of the midbrain. Unfortunately, the progression of this neuronal death has proved difficult to slow and impossible to reverse despite an intense search for the specific causes and for treatments that address the causes. There is a corresponding need to develop approaches that regulate the self-repair mechanisms of neurons, independent of the specific causes of the damage that leads to their death. Red to infrared light therapy (λ=600-1,070 nm) is emerging as an effective, repair-oriented therapy that is capable of stabilizing dying neurons. Initially a space-age anecdote, light therapy has become a treatment for tissue stressed by the known causes of age-related diseases: hypoxia, toxic environments, and mitochondrial dysfunction. Here we focus on several issues relating to the use of light therapy for Parkinson's disease: 1) What is the evidence that it is neuroprotective? We consider the basic science and clinical evidence; 2) What are the mechanisms of neuroprotection? We suggest a primary mechanism acting directly on the neuron's mitochondria (direct effect) as well as a secondary, supportive mechanism acting indirectly through systemic systems (indirect effect); 3) Could this be effective in humans? We discuss the pros and cons of this treatment in humans, including the development of a new surgical method of delivery; and 4) What are the advantages of using light therapy? We explore the features that make this therapy a promising potential treatment. In summary, early evidence indicates that light regulates specific neuronal functions and is neuroprotective in animal models of Parkinson's disease. The stage is set for detailed and rigorous explorations into its use on Parkinson's disease patients, in particular, whether light slows the disease progression rather than simply mitigating signs.

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“…22 Delivered transcranially, 670 nm red light reduces cerebral pathology in animal models of brain damage, Alzheimer's, Parkinson's [23][24][25] and in human ischemic stroke. 26,27 While its mechanism of action remains to be clearly defined, 670 nm red light is thought to be absorbed by cytochrome c oxidase, a rate limiting enzyme in the terminal phosphorylation of the mitochondria.…”

Section: Introductionmentioning

confidence: 99%

A safety and feasibility study of the use of 670 nm red light in premature neonates

et al. 2015

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The impact of near-infrared light on dopaminergic cell survival in a transgenic mouse model of parkinsonism

Cited by 64 publications

References 38 publications

The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

The potential of light therapy in Parkinson's disease

A safety and feasibility study of the use of 670 nm red light in premature neonates

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The impact of near-infrared light on dopaminergic cell survival in a transgenic mouse model of parkinsonism

Cited by 64 publications

References 38 publications

The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

The effect of different doses of near infrared light on dopaminergic cell survival and gliosis in MPTP-treated mice

The potential of light therapy in Parkinson&#39;s disease

A safety and feasibility study of the use of 670 nm red light in premature neonates

Contact Info

Product

Resources

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The potential of light therapy in Parkinson's disease