Mitochondrial Dysfunction and Parkinson’s Disease—Near-Infrared Photobiomodulation as a Potential Therapeutic Strategy

Foo, Aaron Song Chuan; Soong, Tuck Wah; Yeo, Tseng Tsai; Lim, Kah‐Leong

doi:10.3389/fnagi.2020.00089

Cited by 38 publications

(30 citation statements)

References 118 publications

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“…One human pilot trial and one clinical trial of transcranial and intranasal PBM have been conducted to date, which have shown improvements in speech, cognition, gait, and freezing episodes in patients with established PD (Hamilton et al, 2019;Santos et al, 2019). However, the utility of PBM neuroprotection relies on there being neurons to protect in the first instance (Yang et al, 2020), meaning this approach would likely be useful in the early stages of PD with sustained use to moderate disease progression (Foo et al, 2020).…”

Section: Photobiomodulationmentioning

confidence: 99%

Targeting Mitochondrial Impairment in Parkinson's Disease: Challenges and Opportunities

Prasuhn

Davis

Kumar

2021

Front. Cell Dev. Biol.

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The underlying pathophysiology of Parkinson's disease is complex, but mitochondrial dysfunction has an established and prominent role. This is supported by an already large and rapidly growing body of evidence showing that the role of mitochondrial (dys)function is central and multifaceted. However, there are clear gaps in knowledge, including the dilemma of explaining why inherited mitochondriopathies do not usually present with parkinsonian symptoms. Many aspects of mitochondrial function are potential therapeutic targets, including reactive oxygen species production, mitophagy, mitochondrial biogenesis, mitochondrial dynamics and trafficking, mitochondrial metal ion homeostasis, sirtuins, and endoplasmic reticulum links with mitochondria. Potential therapeutic strategies may also incorporate exercise, microRNAs, mitochondrial transplantation, stem cell therapies, and photobiomodulation. Despite multiple studies adopting numerous treatment strategies, clinical trials to date have generally failed to show benefit. To overcome this hurdle, more accurate biomarkers of mitochondrial dysfunction are required to detect subtle beneficial effects. Furthermore, selecting study participants early in the disease course, studying them for suitable durations, and stratifying them according to genetic and neuroimaging findings may increase the likelihood of successful clinical trials. Moreover, treatments involving combined approaches will likely better address the complexity of mitochondrial dysfunction in Parkinson's disease. Therefore, selecting the right patients, at the right time, and using targeted combination treatments, may offer the best chance for development of an effective novel therapy targeting mitochondrial dysfunction in Parkinson's disease.

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Section: Photobiomodulationmentioning

confidence: 99%

Targeting Mitochondrial Impairment in Parkinson's Disease: Challenges and Opportunities

Prasuhn

Davis

Kumar

2021

Front. Cell Dev. Biol.

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“…It has been reported that photobiomodulation (PBM) with light at 808 nm has beneficial effects on damaged mitochondria in cells [ 27 , 28 , 29 , 30 , 31 ]. In recent years, PBM has become an increasingly attractive modality to modulate reactive oxygen species in cells [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

Autophagy and Apoptosis Induced in U87 MG Glioblastoma Cells by Hypericin-Mediated Photodynamic Therapy Can Be Photobiomodulated with 808 nm Light

2021

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Glioblastoma is one of the most aggressive types of tumors. Although few treatment options are currently available, new modalities are needed to improve prognosis. In this context, photodynamic therapy (PDT) is a promising adjuvant treatment modality. In the present work, hypericin-mediated PDT (hypericin-PDT, 2 J/cm2) of U87 MG cells is combined with (2 min, 15 mW/cm2 at 808 nm) photobiomodulation (PBM). We observed that PBM stimulates autophagy, which, in combination with PDT, increases the treatment efficacy and leads to apoptosis. Confocal fluorescence microscopy, cytotoxicity assays and Western blot were used to monitor apoptotic and autophagic processes in these cells. Destabilization of lysosomes, mitochondria and the Golgi apparatus led to an increase in lactate dehydrogenase activity, oxidative stress levels, LC3-II, and caspase-3, as well as a decrease of the PKCα and STAT3 protein levels in response to hypericin-PDT subcellular concentration in U87 MG cells. Our results indicate that therapeutic hypericin concentrations can be reduced when PDT is combined with PBM. This will likely allow to reduce the damage induced in surrounding healthy tissues when PBM-hypericin-PDT is used for in vivo tumor treatments.

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“…Meanwhile, as aggregates of abnormally folded proteins has been identified to be a common pathogenesis of neurodegeneration, the accumulation of intracellular protein inclusions which composes primarily of α-synuclein is found to be an important biological hallmark of PD. Till now, α-synuclein is recognized as a major component to form a variety of different aggregates with thin thread-like or small dot-like structures in the brain with neurodegenerative disease [ 1 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson’s disease model

Ding

et al. 2021

Cell Biosci

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Background ADP/ATP translocase 1 (ANT1) is involved in the exchange of cytosolic ADP and mitochondrial ATP, and its defection plays an important role in mitochondrial pathogenesis. To reveal an etiological implication of ANT1 for Parkinson’s disease (PD), a neurodegenerative disorder, a mouse model treated with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine and neuroblastoma cell model induced by 1-methyl-4-pehny1-pyridine were utilized in this study. Results The tissue-specific abundance in ANT1 in mouse brains was accessed using the analysis of Western blot and immunohistochemistry. Down-regulated soluble ANT1 was found to be correlated with PD, and ANT1 was associated with PD pathogenesis via forming protein aggregates with α-synuclein. This finding was confirmed at cellular level using neuroblastoma cell models. ANT1 supplement in neuronal cells revealed the protective roles of ANT1 against cytotoxicity caused by MPP+. Protein interaction assay, coupled with the analysis of LC-MS/MS, silver-stained SDS-PAGE and Western blot against anti-ANT1 antibody respectively, illustrated the interaction of ANT1 with α-synuclein using the expressed α-synuclein as a bite. Additionally, a significant increasing ROSs was detected in the MPP+-treated cells. Conclusions This study indicated that ANT1 was a potentially causative factor of PD, and led to neuropathogenic injury via promoting the formation of protein aggregates with α-synuclein. This investigation potentially promotes an innovative understanding of ANT1 on the etiology of PD and provides valuable information on developing potential drug targets in PD treatment or reliable biomarkers in PD prognostication.

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Mitochondrial Dysfunction and Parkinson’s Disease—Near-Infrared Photobiomodulation as a Potential Therapeutic Strategy

Cited by 38 publications

References 118 publications

Targeting Mitochondrial Impairment in Parkinson's Disease: Challenges and Opportunities

Targeting Mitochondrial Impairment in Parkinson's Disease: Challenges and Opportunities

Autophagy and Apoptosis Induced in U87 MG Glioblastoma Cells by Hypericin-Mediated Photodynamic Therapy Can Be Photobiomodulated with 808 nm Light

ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson’s disease model

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