The effects of motor rehabilitation training on clinical symptoms and serum BDNF levels in Parkinson’s disease subjects

Gadelha-Filho

Oxidative Medicine and Cellular Longevity

et al. 2017

Parkinson's disease (PD), a progressive neurological pathology, presents motor and nonmotor impairments. The objectives were to support data on exercise benefits to PD. Male Wistar rats were distributed into sham-operated (SO) and 6-OHDA-lesioned, both groups without and with exercise. The animals were subjected to treadmill exercises (14 days), 24 h after the stereotaxic surgery and striatal 6-OHDA injection. Those from no-exercise groups stayed on the treadmill for the same period and, afterwards, were subjected to behavioral tests and euthanized for neurochemical and immunohistochemical assays. The data, analyzed by ANOVA and Tukey post hoc test, were considered significant for p < 0.05. The results showed behavioral change improvements in the 6-OHDA group, after the treadmill exercise, evaluated by apomorphine rotational behavior, open field, and rota rod tests. The exercise reduced striatal dopaminergic neuronal loss and decreased the oxidative stress. In addition, significant increases in BDNF contents and in immunoreactive cells to TH and DAT were also observed, in striata of the 6-OHDA group with exercise, relatively to those with no exercise. We conclude that exercise improves behavior and dopaminergic neurotransmission in 6-OHDA-lesioned animals. The increased oxidative stress and decreased BDNF contents were also reversed, emphasizing the importance of exercise for the PD management.

Section: Discussionsupporting

confidence: 86%

The Treadmill Exercise Protects against Dopaminergic Neuron Loss and Brain Oxidative Stress in Parkinsonian Rats

Gadelha-Filho

Oxidative Medicine and Cellular Longevity

et al. 2017

BioMed Research International

“…Research has shown that in cerebral ischemic rats BDNF/TrkB expression is upregulated to stabilize ischemia-induced Ca 2+ imbalance, inhibit the toxic effect of excitatory amino acids on neurons, and stimulate the survival and regeneration of damaged neurons as well as differentiation and proliferation of neural stem cells [24–26]. Rehabilitation training has been found to increase the expression of BDNF in cerebral ischemia mice [27] and in the serum of patients with Parkinson's disease [28]. On the other hand, resveratrol is shown to increase the expression of Sirt1 as well as BDNF and its receptor TrkB [29] in elderly rats, suggesting that Sirt1 might protect retinal neurons and visual function through the regulation of BDNF/TrkB.…”

Section: Discussionmentioning

confidence: 99%

Rehabilitation Training and Resveratrol Improve the Recovery of Neurological and Motor Function in Rats after Cerebral Ischemic Injury through the Sirt1 Signaling Pathway

Shi

Zhu

2016

This study was conducted to investigate the recovery of motor function in rats through the silent information regulator factor 2-related enzyme 1 (Sirt1) signal pathway-mediated rehabilitation training. Middle cerebral artery occlusion (MACO) was used to induce ischemia/reperfusion injury. The rats were subjected to no treatment (model), rehabilitation training (for 21 days), resveratrol (5 mg/kg for 21 days), and rehabilitation training plus resveratrol treatment. 24 h later, They were assessed for neurobehavioral score and motor behavior score and expression of brain derived-nerve neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB). Compared with sham group, models had significantly higher neurobehavioral scores, balance beam, and rotary stick scores. Compared with the model group, rats in rehabilitation training and resveratrol groups had significantly reduced scores. Compared with rehabilitation training or resveratrol treatment alone, rehabilitation plus resveratrol further reduced the scores significantly. The percentage of cells expressing BDNF and TrkB and expression levels of BDNF and TrkB were similar between the model and sham groups, significantly increased in rehabilitation training and resveratrol groups, and further increased in rehabilitation training plus resveratrol group. These results indicate that rehabilitation raining plus resveratrol can significantly improve the recovery of motor function in rats after cerebral ischemic injury, which is likely related to the upregulation of the BDNF/TrkB signaling pathway.

“…Three studies using blood sampling methods [27,28,33] showed positive results on neuroplasticity after a period of physical exercise. However, a fourth study within the neurochemical domain, Angelucci et al, showed no effects [31]. In the seven studies in which brain function was the main outcome measure, five different methods showed positive effects on neuroplasticity.…”

Section: Studymentioning

confidence: 98%

“…Six studies included participants according to disease stage based on the Hoehn and Yahr scale [25,[28][29][30][31][32] (see Table 1 for study characteristics).…”

Section: Neural Plasticitymentioning

confidence: 99%

“…Seven different methods were used to measure neuroplasticity, and these were further operationalized into three domains: neurochemical (level of brain-derived neurotrophic factor (BDNF) in blood or serum (three studies) [28,31,33] and BDNF-TrkB signaling (one study)) [27], brain function (functional MRI (fMRI) (four studies) [19,32,34,35], electroencephalogram (EEG) (one study) [29], positron emission tomography (PET) (two studies) [26,36], transcranial magnetic stimulation (TMS) (one study)) [25], and brain structure (magnetic resonance imaging (MRI) (one study)) [34]. Assessment details are summarized in Table 1.…”

Section: Outcome Measures Of Neuroplasticitymentioning

confidence: 99%

See 1 more Smart Citation

Exercise-Induced Neuroplasticity in Parkinson’s Disease: A Metasynthesis of the Literature

et al. 2020

Parkinson’s disease (PD) is a neurodegenerative disorder for which there is currently only symptomatic treatment. During the last decade, there has been an increased interest in investigating physical exercise as a neuroprotective mechanism in PD. Animal studies have suggested that exercise may in fact induce neuroplastic changes, but evidence in humans is still scarce. A handful of reviews have previously reported on exercise-induced neuroplasticity in humans with PD, but few have been systematic, or have mixed studies on both animals and humans, or focused on one neuroplastic outcome only. Here, we provide a systematic review and metasynthesis of the published studies on humans in this research field where we have also included different methods of evaluating neuroplasticity. Our results indicate that various forms of physical exercise may lead to changes in various markers of neuroplasticity. A narrative synthesis suggests that brain function and structure can be altered in a positive direction after an exercise period, whereas a meta-analysis on neurochemical adaptations after exercise points in disparate directions. Finally, a GRADE analysis showed that the current overall level of evidence for exercise-induced neuroplasticity in people with PD is very low. Our results demonstrate that even though the results in this area point in a positive direction, researchers need to provide studies of higher quality using more rigorous methodology.