Physical exercise protects against mitochondria alterations in the 6-hidroxydopamine rat model of Parkinson’s disease

Ferreira, Ademar; Binda, Karina Henrique; Singulani, Monique Patrício; Pereira, Carolina Parga Martins; Ferrari, Gustavo Duarte; Alberici, Luciane C.; Real, Caroline Cristiano; Britto, Luiz Roberto

doi:10.1016/j.bbr.2020.112607

Cited by 28 publications

(21 citation statements)

References 56 publications

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“…Furthermore, 4 weeks of exercise prevented a reduction in transcription factor A, mitochondrial (TFAM) and C.I protein levels and augmented C.I activity. This suggests that intermittent exercise improves mitochondrial biogenesis signalling and respiratory chain modulation of the dopaminergic system in PD (Fernandes Ferreira et al, 2020).…”

Section: Exercisementioning

confidence: 88%

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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: Exercisementioning

confidence: 88%

“…In a unilateral PD rat model, rats were subjected to either 1 or 4 weeks intermittent moderate treadmill exercise (Fernandes Ferreira et al, 2020). The investigators showed that 1 week of exercise prevented a decrease in peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) and NRF-1 expression.…”

Section: Exercisementioning

confidence: 99%

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

Prasuhn

Davis

Kumar

2021

Front. Cell Dev. Biol.

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Section: Effects Of Te Training On Neural Mitochondrial Respiratory Deficiency In Pdmentioning

confidence: 99%

“…Three studies analyzed the effects of TE training on mitochondrial complex I in PD [15,23,26]. Two of those showed that the protein levels of complex I were reduced in PD compared to normal, whereas TE training enhanced their levels in PD [15,26]. However, the other study observed that the protein levels of complex I were similar among the normal control group, the PD group, and the TE-trained PD group [23].…”

Section: Effects Of Te Training On Neural Mitochondrial Respiratory Deficiency In Pdmentioning

confidence: 99%

“…Five authors accessed the expression of complexes II, III, IV, and V, reporting different results [15,20,21,23,26]. One study reported that the protein levels of complexes II, III, IV, and V were unchanged among the normal control group, the sedentary PD group, and the TE-trained PD group [26].…”

Section: Effects Of Te Training On Neural Mitochondrial Respiratory Deficiency In Pdmentioning

confidence: 99%

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Effects of Treadmill Exercise on Neural Mitochondrial Functions in Parkinson’s Disease: A Systematic Review of Animal Studies

2021

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This systematic review sought to determine the effects of treadmill exercise on the neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease. PubMed, Web of Science, and EMBASE databases were searched through March 2020. The English-published animal studies that mentioned the effects of treadmill exercise on neural mitochondria in Parkinson’s disease were included. The CAMARADES checklist was used to assess the methodological quality of the studies. Ten controlled trials were included (median CAMARADES score = 5.7/10) with various treadmill exercise durations (1–18 weeks). Seven studies analyzed the neural mitochondrial respiration, showing that treadmill training attenuated complex I deficits, cytochrome c release, ATP depletion, and complexes II–V abnormalities in Parkinson’s disease. Nine studies analyzed the neural mitochondrial quality-control, reporting that treadmill exercise improved mitochondrial biogenesis, mitochondrial fusion, and mitophagy in Parkinson’s disease. The review findings supported the hypothesis that treadmill training could attenuate both neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease, suggesting that treadmill training might slow down the progression of Parkinson’s disease.

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The Hypoxia Response Pathway: A Potential Intervention Target in Parkinson's Disease?

Janssen Daalen,

Koopman,

Saris

et al. 2023

Movement Disorders

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Parkinson's disease (PD) is a progressive neurodegenerative disorder for which only symptomatic treatments are available. Both preclinical and clinical studies suggest that moderate hypoxia induces evolutionarily conserved adaptive mechanisms that enhance neuronal viability and survival. Therefore, targeting the hypoxia response pathway might provide neuroprotection by ameliorating the deleterious effects of mitochondrial dysfunction and oxidative stress, which underlie neurodegeneration in PD. Here, we review experimental studies regarding the link between PD pathophysiology and neurophysiological adaptations to hypoxia. We highlight the mechanistic differences between the rescuing effects of chronic hypoxia in neurodegeneration and short‐term moderate hypoxia to improve neuronal resilience, termed “hypoxic conditioning”. Moreover, we interpret these preclinical observations regarding the pharmacological targeting of the hypoxia response pathway. Finally, we discuss controversies with respect to the differential effects of hypoxia response pathway activation across the PD spectrum, as well as intervention dosing in hypoxic conditioning and potential harmful effects of such interventions. We recommend that initial clinical studies in PD should focus on the safety, physiological responses, and mechanisms of hypoxic conditioning, as well as on repurposing of existing pharmacological compounds. © 2023 International Parkinson and Movement Disorder Society.

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Physical exercise protects against mitochondria alterations in the 6-hidroxydopamine rat model of Parkinson’s disease

Cited by 28 publications

References 56 publications

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

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

Effects of Treadmill Exercise on Neural Mitochondrial Functions in Parkinson’s Disease: A Systematic Review of Animal Studies

The Hypoxia Response Pathway: A Potential Intervention Target in Parkinson's Disease?

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