Special Issue "Photobiomodulation for Parkinson's Disease"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 6 December 2019.

Special Issue Editor

Prof. John Mitrofanis
E-Mail Website
Guest Editor
University of Sydney, Australia
Interests: Parkinson's disease; basal ganglia circuitry; neuroprotection

Special Issue Information

Dear Colleagues,

Parkinson's disease is a neurological disorder with cardinal signs of resting tremor, akinesia, bradykinesia, lead-pipe rigidity, and postural instability. Two key features of the disease are that there is a rather targeted degeneration of a particular neurotransmitter system (i.e., dopaminergic) and that this degeneration is progressive, with more and more neurones dying over time. The current treatments are effective in treating motor signs, but not, however, in slowing the relentless progression of the degeneration. Recently, photobiomodulation—the use of red to near-infrared light on body tissues—has been reported to slow this neurodegeneration in a range of animal models, from flies to monkeys. There are also some encouraging, early reports that photobiomodulation results in many beneficial outcomes in patients. This Special Issue will explore various aspects of this new and exciting treatment in animal models and in patients, building on the template of findings needed to develop this treatment into a viable therapeutic option for patients. 

Prof. John Mitrofanis
Guest Editor

Manuscript Submission Information

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Keywords

  • Parkinson's disease
  • neurodegeneration
  • neuroprotection
  • microbiome
  • dopamine
  • red to near-infrared light
  • animal models
  • patients
  • fMRI

Published Papers (2 papers)

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Research

Open AccessArticle
Photobiomodulation Mitigates Cerebrovascular Leakage Induced by the Parkinsonian Neurotoxin MPTP
Biomolecules 2019, 9(10), 564; https://doi.org/10.3390/biom9100564 - 04 Oct 2019
Abstract
The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is commonly used to model Parkinson’s disease (PD) as it specifically damages the nigrostriatal dopaminergic pathway. Recent studies in mice have, however, provided evidence that MPTP also compromises the integrity of the brain’s vasculature. Photobiomodulation (PBM), the irradiation of [...] Read more.
The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is commonly used to model Parkinson’s disease (PD) as it specifically damages the nigrostriatal dopaminergic pathway. Recent studies in mice have, however, provided evidence that MPTP also compromises the integrity of the brain’s vasculature. Photobiomodulation (PBM), the irradiation of tissue with low-intensity red light, mitigates MPTP-induced loss of dopaminergic neurons in the midbrain, but whether PBM also mitigates MPTP-induced damage to the cerebrovasculature has not been investigated. This study aimed to characterize the time course of cerebrovascular disruption following MPTP exposure and to determine whether PBM can mitigate this disruption. Young adult male C57BL/6 mice were injected with 80 mg/kg MPTP or isotonic saline and perfused with fluorescein isothiocyanate FITC-labelled albumin at various time points post-injection. By 7 days post-injection, there was substantial and significant leakage of FITC-labelled albumin into both the substantia nigra pars compacta (SNc; p < 0.0001) and the caudate-putamen complex (CPu; p ≤ 0.0003); this leakage partly subsided by 14 days post-injection. Mice that were injected with MPTP and treated with daily transcranial PBM (670 nm, 50 mW/cm2, 3 min/day), commencing 24 h after MPTP injection, showed significantly less leakage of FITC-labelled albumin in both the SNc (p < 0.0001) and CPu (p = 0.0003) than sham-treated MPTP mice, with levels of leakage that were not significantly different from saline-injected controls. In summary, this study confirms that MPTP damages the brain’s vasculature, delineates the time course of leakage induced by MPTP out to 14 days post-injection, and provides the first direct evidence that PBM can mitigate this leakage. These findings provide new understanding of the use of the MPTP mouse model as an experimental tool and highlight the potential of PBM as a therapeutic tool for reducing vascular dysfunction in neurological conditions. Full article
(This article belongs to the Special Issue Photobiomodulation for Parkinson's Disease)
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Open AccessFeature PaperArticle
Effect of Photobiomodulation in Rescuing Lipopolysaccharide-Induced Dopaminergic Cell Loss in the Male Sprague–Dawley Rat
Biomolecules 2019, 9(8), 381; https://doi.org/10.3390/biom9080381 - 19 Aug 2019
Abstract
Photobiomodulation (PBM) provides neuroprotection against dopaminergic cell death and associated motor deficits in rodent and primate models of Parkinson’s disease (PD). However, it has not yet been tested in the lipopolysaccharide (LPS) model of PD, which leads to dopaminergic cell death through microglia-evoked [...] Read more.
Photobiomodulation (PBM) provides neuroprotection against dopaminergic cell death and associated motor deficits in rodent and primate models of Parkinson’s disease (PD). However, it has not yet been tested in the lipopolysaccharide (LPS) model of PD, which leads to dopaminergic cell death through microglia-evoked neuroinflammation. We investigated whether transcranial PBM could protect against dopaminergic cell death within the substantia nigra in male Sprague–Dawley rats following supranigral LPS injection. PBM fully protected rats from 10 µg LPS which would have otherwise caused 15% cell loss, but there was no significant neuroprotection at a 20 µg dose that led to a 50% lesion. Cell loss at this dose varied according to the precise site of injection and correlated with increased local numbers of highly inflammatory amoeboid microglia. Twenty microgram LPS caused motor deficits in the cylinder, adjusted stepping and rotarod tests that correlated with dopaminergic cell loss. While PBM caused no significant improvement at the group level, motor performance on all three tests no longer correlated with the lesion size caused by 20 µg LPS in PBM-treated rats, suggesting extranigral motor improvements in some animals. These results provide support for PBM as a successful neuroprotective therapy against the inflammatory component of early PD, provided inflammation has not reached a devastating level, as well as potential benefits in other motor circuitries. Full article
(This article belongs to the Special Issue Photobiomodulation for Parkinson's Disease)
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