Effects of mild running on substantia nigra during early neurodegeneration

Almeida, Michael F.; Silva, Carolliny M.; Chaves, Rodrigo S.; Lima, Nathan C.R.; Almeida, Renato S.; Melo, Karla P.; Demasi, Marilene; Fernandes, Tiago; Oliveira, Edilamar Menezes de; Netto, Luís Eduardo Soares; Cardoso, Sandra M.; Ferrari, Merari F. R.

doi:10.1080/02640414.2017.1378494

Cited by 25 publications

(13 citation statements)

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“…Huang et al show that 8-week running exercise in mice can activate the autophagy pathway and improve lysosomal biogenesis, suggesting improvement in brain function of mice; besides that, they also observed that prolonged physical exercise promoted nuclear translocation of transcription factor EB (TFEB-main regulator of autophagic and lysosomal biogenesis) in the cortex, positively regulating the transcription of genes associated with autophagy and lysosome (lysosomal degradation is a fundamental step to completing the autophagy process) (188). It has also been observed that moderate exercise contributes to the prevention of early neurodegeneration in the substantia nigra region in aged rats by improving autophagy and mitophagy (189).…”

Section: Influence Of Physical Exercise In the Autophagy Process In Amentioning

confidence: 96%

Effects of Physical Exercise on Autophagy and Apoptosis in Aged Brain: Human and Animal Studies

et al. 2020

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The aging process is characterized by a series of molecular and cellular changes over the years that could culminate in the deterioration of physiological parameters important to keeping an organism alive and healthy. Physical exercise, defined as planned, structured and repetitive physical activity, has been an important force to alter physiology and brain development during the process of human beings' evolution. Among several aspects of aging, the aim of this review is to discuss the balance between two vital cellular processes such as autophagy and apoptosis, based on the fact that physical exercise as a non-pharmacological strategy seems to rescue the imbalance between autophagy and apoptosis during aging. Therefore, the effects of different types or modalities of physical exercise in humans and animals, and the benefits of each of them on aging, will be discussed as a possible preventive strategy against neuronal death.

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Section: Influence Of Physical Exercise In the Autophagy Process In Amentioning

confidence: 96%

Effects of Physical Exercise on Autophagy and Apoptosis in Aged Brain: Human and Animal Studies

et al. 2020

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“…Current knowledge about the mechanism of the neuroprotective properties of physical training on the functional state of dopaminergic neurons is based on data obtained from animal studies. Many of these studies suggest that exercise can prevent or slow down neurodegenerative processes and rebuild disturbed signaling pathways [11–13]. The neuroprotective effect of physical training is associated with the activation of the neurotrophin signaling pathways [14, 15], synaptogenesis [16], angiogenesis [17] and neurogenesis strengthening [18, 19], reduction of inflammatory processes [20–22], and stabilization of calcium homeostasis [23].…”

Section: Introductionmentioning

confidence: 99%

Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease

et al. 2019

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Physical training confers protection to dopaminergic neurons in rodent models of parkinsonism produced by neurotoxins. The sparing effect of physical training on dopaminergic neurons can be tested with training applied during chronic MPTP treatment, while the neurorestorative effect when training is applied after completing such treatment. In this study, the effect of the onset of training respective to chronic MPTP treatment was specifically addressed. Three groups of mice were injected with 10 doses of MPTP (12.5 mg/kg/injection) over 5 weeks. The first group remained sedentary; the second one underwent early onset training, which started 1 week before commencing MPTP treatment, continued throughout 5 weeks of treatment and 4 weeks thereafter; the third group underwent late-onset training of the same length and intensity as the former group, except that it started immediately after the end of MPTP treatment. Two groups served as controls: a saline-injected group that remained sedentary and saline-injected group, which underwent the same training as the early and late-onset training groups. Both early and late-onset physical training saved almost all nigral and VTA dopaminergic neurons, prevented inflammatory response, and increased the BDNF and GDNF levels to a similar extent. From these results one may conclude that early and late-onset training schedules were equipotent in their neuroprotective effect and that the mechanism of neuroprotection was similar. The sparing effect of early onset training may be satisfactorily explained by assuming that the increased level of BDNF and GDNF prevented the degeneration of dopaminergic neurons. To explain a similar number of dopaminergic neurons detected at the end of the early and late-onset training, one should additionally assume that the former training schedule induced neurogenesis. Results of this study support the view that physical activity may be neuroprotective even at a more advanced stage of PD and justify starting physical activity at any point of the disease.

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“…Using the rotenone model, it has been shown that early aerobic exercise for 2 or 6 weeks was effective to prevent elevated αsynuclein levels while increasing tyrosine hydroxylase levels in the substantia nigra. 36,37 In addition, aerobic exercise for 2 weeks following rotenone exposure was found to reduce the loss of serotonergic markers in the dorsal raphe and mitigate depressive behaviors. 38 Rats that receive aerobic exercise following rotenone exposure also demonstrate improved motor performance in the rotarod test compared to sedentary rats, 37 suggesting preservation of motor function in exercising animals.…”

Section: Rationale For Neuroprotective Effects Of Exercise In Prodrommentioning

confidence: 99%

“…In summary, evidence from aerobic exercise trials in early PD, as well as in parkinsonian animal models, suggests that aerobic exercise may impart beneficial effects on motor function by preserving dopaminergic and corticostriatal systems in the presence of disease. 36,37,46 For a review of aerobic exercise in PD, please see Schootemeijer et al 32 Prescription of aerobic exercise in iRBD should include factors of intensity, duration, and frequency. Moderate-to high-intensity exercise with a duration of 30 to 45 minutes a minimum of 3 times per week is recommended.…”

Section: Exercise As An Intervention For Prodromal Synucleinopathymentioning

confidence: 99%

Motor Dysfunction in REM Sleep Behavior Disorder: A Rehabilitation Framework for Prodromal Synucleinopathy

Summers

Rafferty

Howell

et al. 2021

Neurorehabil Neural Repair

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Parkinson disease (PD) and other related diseases with α-synuclein pathology are associated with a long prodromal or preclinical stage of disease. Predictive models based on diagnosis of idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) make it possible to identify people in the prodromal stage of synucleinopathy who have a high probability of future disease and provide an opportunity to implement neuroprotective therapies. However, rehabilitation providers may be unaware of iRBD and the motor abnormalities that indicate early motor system dysfunction related to α-synuclein pathology. Furthermore, there is no existing rehabilitation framework to guide early interventions for people with iRBD. The purpose of this work is to (1) review extrapyramidal signs of motor system dysfunction in people with iRBD and (2) propose a framework for early protective or preventive therapies in prodromal synucleinopathy using iRBD as a predictive marker. Longitudinal and cross-sectional studies indicate that the earliest emerging motor deficits in iRBD are bradykinesia, deficits performing activities of daily living, and abnormalities in speech, gait, and posture. These deficits may emerge up to 12 years before a diagnosis of synucleinopathy. The proposed rehabilitation framework for iRBD includes early exercise-based interventions of aerobic exercise, progressive resistance training, and multimodal exercise with rehabilitation consultations to address exercise prescription, progression, and monitoring. This rehabilitation framework may be used to implement neuroprotective, multidisciplinary, and proactive clinical care in people with a high likelihood of conversion to PD, dementia with Lewy bodies, or multiple systems atrophy.

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Effects of mild running on substantia nigra during early neurodegeneration

Cited by 25 publications

References 50 publications

Effects of Physical Exercise on Autophagy and Apoptosis in Aged Brain: Human and Animal Studies

Effects of Physical Exercise on Autophagy and Apoptosis in Aged Brain: Human and Animal Studies

Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease

Motor Dysfunction in REM Sleep Behavior Disorder: A Rehabilitation Framework for Prodromal Synucleinopathy

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