CONTEXT:Many researchers are interested in the Eastern therapeutic exercise of qigong and tai chi, performed as qigong. A review of systematic studies through April 2010 found evidence supporting tai chi as effective for preventing falls, improving psychological health, and promoting healthy aging.

OBJECTIVE:The review intended to provide an updated survey of recent systematic reviews to establish the current-2016-level of scientific evidence assessing the therapeutic benefits of qigong exercise for clinical applications related to physical health.

METHODS:The data sources included PubMed, SCOPUS, and CINAHL, using the major terms qigong OR tai chi AND review. Studies were included in the review if they (1) were systematic reviews and meta-analyses; (2) had been published as full text in the English language; (3) were published between January 2010 and December 2016; (4) had tai chi or qigong as the primary intervention of interest; (5) addressed a defined, physical-health complaint; and (6) included≥3 randomized clinical trials. Reviews addressing nonclinical topics, mental health, and cognition were excluded.

RESULTS:The extensive search identified 41 relevant systematic reviews and meta-analyses. Five areas of clinical application were supported. The review showed independent research evidence that was sufficient to support tai chi performed as qigong as a primary intervention for balance training and fall prevention. When compared with more traditional interventions, tai chi was found to have equal, and in some instances, superior effects, as well as cost-effectiveness. In addition, qigong, and tai chi performed as qigong, were found to have a complementary or alternative role in management of cancer, chronic obstructive pulmonary disease, Parkinson's disease, and cardiac and cardiovascular disorders.

CONCLUSIONS:A growing body of evidence supports qigong and tai chi performed as qigong as valid complementary or alternative therapeutic exercises. Many aspects of the clinical study and application in this area remain to be explored.

BACKGROUND: Inflammatory cytokine levels are often elevated in people with Parkinson's disease (PD). People with PD often experience sleep disturbances that significantly impact quality of life. Past studies suggest inflammatory cytokines may be associated with various symptoms of PD. Benefits of Qigong, a mind-body exercise, have been shown in different neurological conditions, but there is still a lack of clinical evidence in the PD population.

METHODS: Ten people with PD were recruited and randomly assigned into two groups receiving six weeks of Qigong (experimental group) or sham Qigong (control group) intervention. The levels of TNF-α, IL-1β, and IL-6 in subjects' serum and sleep quality were measured before and after the intervention.

RESULTS: After the intervention, the serum level of TNF-α in the experimental group was significantly decreased in all subjects, while the level in the control group showed a trend to increase. Qigong exercise significantly improved sleep quality at night. There was a strong correlation between changes in the level of TNF-α and sleep quality.

CONCLUSION: Qigong exercise decreased TNF-α level in people with PD and helped improve sleep quality. TNF-α may have a potential to influence the sleep quality in people with PD.

OBJECTIVES: Parkinson's disease is a complex disease with multiple etiological factors involved in disease pathogenesis, and the molecular and cellular pathways for neurodegeneration are still elusive. METHODS: We reviewed all the relevant laboratory findings regarding acupuncture mechanism on Parkinson's disease. RESULTS: Acupuncture treatments in animal experiments have generated valuable mechanistic insights of Parkinson's disease and shown that acupuncture therapy is in fact a neuroprotective therapy which increases various neuroprotective agents such as brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor and cyclophilin A. In addition, acupuncture therapy decreases cell death processes and attenuates oxidative stress to substantia nigra dopaminergic neurons. DISCUSSION: These results suggest that early application of acupuncture therapy for Parkinson's disease patients may be helpful for the best efficacy of acupuncture treatment.

OBJECTIVES: Parkinson's disease is a complex disease with multiple etiological factors involved in disease pathogenesis, and the molecular and cellular pathways for neurodegeneration are still elusive. METHODS: We reviewed all the relevant laboratory findings regarding acupuncture mechanism on Parkinson's disease. RESULTS: Acupuncture treatments in animal experiments have generated valuable mechanistic insights of Parkinson's disease and shown that acupuncture therapy is in fact a neuroprotective therapy which increases various neuroprotective agents such as brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor and cyclophilin A. In addition, acupuncture therapy decreases cell death processes and attenuates oxidative stress to substantia nigra dopaminergic neurons. DISCUSSION: These results suggest that early application of acupuncture therapy for Parkinson's disease patients may be helpful for the best efficacy of acupuncture treatment.

Free radical mediated damage has been reported to contribute significantly towards low survival (5-10%) of grafted dopaminergic neurons, post transplantation. In the present study, an attempt has been made to explore the neuroprotective potential of the combination of two major antioxidants ascorbic acid (AA) and glutathione (GSH) on ventral mesencephalic cells (VMC) and nigral dopamine (DA) neurons when co-transplanted together with VMC in rat model of Parkinson's disease (PD). GSH and AA have been reported to act co-operatively in the conditions of oxidative stress thereby helping in maintaining the cellular GSH/GSSG redox status. Functional recovery was assessed 12 weeks post transplantation, where a significant restoration (p<0.001) in d-amphetamine induced circling behavior (62%), spontaneous locomotor activity (SLA; 64%), dopamine-D2 receptor binding (63%), dopamine (65%) and 3,4-dihydroxy phenyl acetic acid (DOPAC) level (64%) was observed in co-transplanted animals as compared to lesioned and VMC alone grafted rats. VMC and GSH+AA co-transplanted animals exhibited a significantly higher surviving TH-immunoreactive (TH-ir) neurons number (p<0.01), TH-ir fibers outgrowth (p<0.05) in striatal graft and TH-ir neurons in substantia nigra pars compacta (SNpc) (p<0.01), as compared to VMC alone transplanted rats. An attempt was made to further confirm our in vivo observations through in vitro experiments where following in vitro exposure to 6-OHDA, a higher cell survival (p<0.01), TH-ir cell counts (p<0.001) and DA and DOPAC levels (p<0.01) were also observed in 8-day-old VMC culture in presence of GSH+AA as compared to VMC cultured in absence of antioxidants. The results suggest that GSH+AA when co-transplanted with VMC provide higher restoration probably by increasing the survival of grafted VMC and simultaneously supporting nigral TH-immunopositive neurons in rat model of PD.

Free radical mediated damage has been reported to contribute significantly towards low survival (5-10%) of grafted dopaminergic neurons, post transplantation. In the present study, an attempt has been made to explore the neuroprotective potential of the combination of two major antioxidants ascorbic acid (AA) and glutathione (GSH) on ventral mesencephalic cells (VMC) and nigral dopamine (DA) neurons when co-transplanted together with VMC in rat model of Parkinson's disease (PD). GSH and AA have been reported to act co-operatively in the conditions of oxidative stress thereby helping in maintaining the cellular GSH/GSSG redox status. Functional recovery was assessed 12 weeks post transplantation, where a significant restoration (p<0.001) in d-amphetamine induced circling behavior (62%), spontaneous locomotor activity (SLA; 64%), dopamine-D2 receptor binding (63%), dopamine (65%) and 3,4-dihydroxy phenyl acetic acid (DOPAC) level (64%) was observed in co-transplanted animals as compared to lesioned and VMC alone grafted rats. VMC and GSH+AA co-transplanted animals exhibited a significantly higher surviving TH-immunoreactive (TH-ir) neurons number (p<0.01), TH-ir fibers outgrowth (p<0.05) in striatal graft and TH-ir neurons in substantia nigra pars compacta (SNpc) (p<0.01), as compared to VMC alone transplanted rats. An attempt was made to further confirm our in vivo observations through in vitro experiments where following in vitro exposure to 6-OHDA, a higher cell survival (p<0.01), TH-ir cell counts (p<0.001) and DA and DOPAC levels (p<0.01) were also observed in 8-day-old VMC culture in presence of GSH+AA as compared to VMC cultured in absence of antioxidants. The results suggest that GSH+AA when co-transplanted with VMC provide higher restoration probably by increasing the survival of grafted VMC and simultaneously supporting nigral TH-immunopositive neurons in rat model of PD.

A wide range of neurodegenerative diseases (NDs), including Alzheimer's disease, Parkinson's disease, Huntington's disease, and prion diseases, share common mechanisms such as neuronal loss, apoptosis, mitochondrial dysfunction, oxidative stress, and inflammation. Intervention strategies using plant-derived bioactive compounds have been offered as a form of treatment for these debilitating conditions, as there are currently no remedies to prevent, reverse, or halt the progression of neuronal loss. Rutin, a glycoside of the flavonoid quercetin, is found in many plants and fruits, especially buckwheat, apricots, cherries, grapes, grapefruit, plums, and oranges. Pharmacological studies have reported the beneficial effects of rutin in many disease conditions, and its therapeutic potential in several models of NDs has created considerable excitement. Here, we have summarized the current knowledge on the neuroprotective mechanisms of rutin in various experimental models of NDs. The mechanisms of action reviewed in this article include reduction of proinflammatory cytokines, improved antioxidant enzyme activities, activation of the mitogen-activated protein kinase cascade, downregulation of mRNA expression of PD-linked and proapoptotic genes, upregulation of the ion transport and antiapoptotic genes, and restoration of the activities of mitochondrial complex enzymes. Taken together, these findings suggest that rutin may be a promising neuroprotective compound for the treatment of NDs.

OBJECTIVE: The goal of this pilot study was to determine the effects of short duration, intensive tango lessons on functional mobility in people with Parkinson disease. DESIGN: This study employed a within-subject, prospective, repeated measures design.

SUBJECTS/PATIENTS: Fourteen people with idiopathic Parkinson disease participated. SETTING: All balance and gait assessments were performed in a laboratory, but dance classes took place in a large, open classroom.

INTERVENTIONS: Participants completed ten 1.5-h long Argentine tango dance lessons within 2 weeks. Their balance, gait and mobility were assessed before and after the training sessions.

MAIN OUTCOME MEASURES: Measures included the Berg Balance Scale, the Unified Parkinson Disease Rating Scale, gait velocity, functional ambulation profile, step length, stance and single support percent of gait, Timed Up and Go, and the 6 min walk.

RESULTS: Participants significantly improved on the Berg Balance Scale (effect size (ES)=0.83, p=0.021), Unified Parkinson Disease Rating Scale Motor Subscale III (ES=-0.64, p=0.029), and percent of time spent in stance during forward walking (ES=0.97, p=0.015). Non-significant improvements were noted on the Timed Up and Go (ES=-0.38, p=0.220) and 6 min walk (ES=0.35, p=0.170).

CONCLUSIONS: Frequent social dance lessons completed within a short time period appear to be appropriate and effective for these individuals with mild-moderately severe Parkinson disease.

We applied rhythmic binaural sound to Parkinson's Disease (PD) patients to investigate its influence on several symptoms of this disease and on Electrophysiology (Electrocardiography and Electroencephalography (EEG)). We conducted a double-blind, randomized controlled study in which rhythmic binaural beats and control were administered over two randomized and counterbalanced sessions (within-subjects repeated-measures design). Patients ([Formula: see text], age [Formula: see text], stage I-III Hoehn&Yahr scale) participated in two sessions of sound stimulation for 10[Formula: see text]min separated by a minimum of 7 days. Data were collected immediately before and after both stimulations with the following results: (1) a decrease in theta activity, (2) a general decrease in Functional Connectivity (FC), and (3) an improvement in working memory performance. However, no significant changes were identified in the gait performance, heart rate or anxiety level of the patients. With regard to the control stimulation, we did not identify significant changes in the variables analyzed. The use of binaural-rhythm stimulation for PD, as designed in this study, seems to be an effective, portable, inexpensive and noninvasive method to modulate brain activity. This influence on brain activity did not induce changes in anxiety or gait parameters; however, it resulted in a normalization of EEG power (altered in PD), normalization of brain FC (also altered in PD) and working memory improvement (a normalizing effect). In summary, we consider that sound, particularly binaural-rhythmic sound, may be a co-assistant tool in the treatment of PD, however more research is needed to consider the use of this type of stimulation as an effective therapy.

BACKGROUND:Patients with Parkinson's disease have substantially impaired balance, leading to diminished functional ability and an increased risk of falling. Although exercise is routinely encouraged by health care providers, few programs have been proven effective.

METHODS:We conducted a randomized, controlled trial to determine whether a tailored tai chi program could improve postural control in patients with idiopathic Parkinson's disease. We randomly assigned 195 patients with stage 1 to 4 disease on the Hoehn and Yahr staging scale (which ranges from 1 to 5, with higher stages indicating more severe disease) to one of three groups: tai chi, resistance training, or stretching. The patients participated in 60-minute exercise sessions twice weekly for 24 weeks. The primary outcomes were changes from baseline in the limits-of-stability test (maximum excursion and directional control; range, 0 to 100%). Secondary outcomes included measures of gait and strength, scores on functional-reach and timed up-and-go tests, motor scores on the Unified Parkinson's Disease Rating Scale, and number of falls.

RESULTS:The tai chi group performed consistently better than the resistance-training and stretching groups in maximum excursion (between-group difference in the change from baseline, 5.55 percentage points; 95% confidence interval [CI], 1.12 to 9.97; and 11.98 percentage points; 95% CI, 7.21 to 16.74, respectively) and in directional control (10.45 percentage points; 95% CI, 3.89 to 17.00; and 11.38 percentage points; 95% CI, 5.50 to 17.27, respectively). The tai chi group also performed better than the stretching group in all secondary outcomes and outperformed the resistance-training group in stride length and functional reach. Tai chi lowered the incidence of falls as compared with stretching but not as compared with resistance training. The effects of tai chi training were maintained at 3 months after the intervention. No serious adverse events were observed.

CONCLUSIONS:Tai chi training appears to reduce balance impairments in patients with mild-to-moderate Parkinson's disease, with additional benefits of improved functional capacity and reduced falls. (Funded by the National Institute of Neurological Disorders and Stroke; ClinicalTrials.gov number, NCT00611481.).

This pilot study examines the effects of Tai Chi on balance, gait and mobility in people with Parkinson disease (PD). Thirty-three people with PD were randomly assigned to either a Tai Chi group or a control group. The Tai Chi group participated in 20 1-h long training sessions completed within 10-13 weeks; whereas, the control group had two testing sessions between 10 and 13 weeks apart without interposed training. The Tai Chi group improved more than the control group on the Berg Balance Scale, UPDRS, Timed Up and Go, tandem stance test, six-minute walk, and backward walking. Neither group improved in forward walking or the one leg stance test. All Tai Chi participants reported satisfaction with the program and improvements in well-being. Tai Chi appears to be an appropriate, safe and effective form of exercise for some individuals with mild-moderately severe PD.

Parkinson's disease (PD) is a significantly progressive neurodegenerative disease characterised by both motor and nonmotor disorders. The main pathological characteristics of PD consist of the loss of dopaminergic neurons and the formation of alpha-synuclein-containing Lewy bodies in the substantia nigra. Currently, the main therapeutic method for PD is anti-Parkinson medications, including levodopa, madopar, sirelin, and so on. However, the effect of pharmacological treatment has its own limitations, the most significant of which is that the therapeutic effect of dopaminergic treatments gradually diminishes with time. Exercise training, as an adjunctive treatment and complementary therapy, can improve the plasticity of cortical striatum and increase the release of dopamine. Exercise training has been proven to effectively improve motor disorders (including balance, gait, risk of falls and physical function) and nonmotor disorders (such as sleep impairments, cognitive function and quality of life) in PD patients. In recent years, various types of exercise training have been used to treat PD. In this review, we summarise the exercise therapy mechanisms and the protective effects of different types of exercise training on PD patients.

Electroacupuncture (EA) has been reported to alleviate motor deficits in Parkinson's disease (PD) patients, and PD animal models. However, the mechanisms by which EA improves motor function have not been investigated. We have employed a 6-hydroxydopamine (6-OHDA) unilateral injection induced PD model to investigate whether EA alters protein expression in the motor cortex. We found that 4 weeks of EA treatment significantly improved spontaneous floor plane locomotion and rotarod performance. High-throughput proteomic analysis in the motor cortex was employed. The expression of 54 proteins were altered in the unlesioned motor cortex, and 102 protein expressions were altered in the lesioned motor cortex of 6-OHDA rats compared to sham rats. Compared to non-treatment PD control, EA treatment reversed 6 proteins in unlesioned and 19 proteins in lesioned motor cortex. The present study demonstrated that PD induces proteomic changes in the motor cortex, some of which are rescued by EA treatment. These targeted proteins were mainly involved in increasing autophagy, mRNA processing and ATP binding and maintaining the balance of neurotransmitters.

Parkinson's disease is characterized by neurodegeneration and learning deficiency. Physical exercise can alleviate these symptoms by increasing the expression of some effective and relevant factors. The preventive effect of 16-week treadmill running in a rat model of Parkinson's disease, before 6-hydroxydopamine (6-OHDA) induction, was assessed. Experimental groups consisted of sedentary (SED), SED+6-OHDA, exercised (EX), and EX+6-OHDA rats. Forty-eight hours after the last session of exercise, 6-OHDA was injected into the medial forebrain bundle (MFB). One week after the injection, behavioral tests, including spatial learning and memory, were assessed through Morris water maze (MWM) and apomorphine-induced rotation. Three weeks after the injection, mRNA expression and protein levels of the transcriptional co-activator peroxisome-proliferator-activated receptor-γ co-activator-1α (), fibronectin type III domain-containing protein 5 (), brain-derived neurotrophic factor (), and tyrosine hydroxylase () were measured in the striatum and the hippocampus of rats by applying real-time PCR and Western blotting. The findings indicate that exposure to 6-OHDA leads to impairments in behavioral and molecular functions. Exercise training prevents and reduces the symptoms caused by dopamine toxins. The results suggest that treadmill running can exert neuroprotective and have preventive effects to reduce Parkinson's disease symptoms.Parkinson's disease impairs spatial learning and memory. Parkinson's disease reduced levels of,, andand increased neurodegeneration in the striatum and the hippocampus. Treadmill running before disease attenuated 6-OHDA-induced memory deficit and elevated neuroprotection. Exercise has multiple effects on memory and biochemical factors.

The present systematic review is based on the premise that a variety of neurodegenerative diseases are accompanied by grey matter atrophy in the brain and meditation may impact this. Given that age is a major risk factor for many of these progressive and neurodegenerative diseases and that the percentage of the population over the age of 65 is quickly increasing, there is an obvious need for prompt treatment and prevention advances in research. As there is currently no cure for Alzheimer's disease and other neurodegenerative diseases, many are seeking non-pharmacological treatment options in attempts to offset the disease-related cognitive and functional declines. On the basis of a growing body of research suggesting that meditation is effective in increasing grey matter volume in healthy participants, this paper systematically reviewed the literature regarding the effects of meditation on restoring grey matter volume in healthy individuals and those affected by neurodegeneration. This review searched PubMed, CINAHL, and APA PsycNET to identify original studies that included MRI imaging to measure grey matter volume in meditators and post-mindfulness-based intervention participants compared to controls. Thirteen studies were considered eligible for review and involved a wide variety of meditation techniques and included participants with and without cognitive impairment. All studies reported significant increases in grey matter volume in the meditators/intervention group, albeit in assorted regions of the brain. Limited research exists on the mechanisms through which meditation affects disease-related neurodegeneration, but preliminary evidence suggests that it may offset grey matter atrophy.

The present systematic review is based on the premise that a variety of neurodegenerative diseases are accompanied by grey matter atrophy in the brain and meditation may impact this. Given that age is a major risk factor for many of these progressive and neurodegenerative diseases and that the percentage of the population over the age of 65 is quickly increasing, there is an obvious need for prompt treatment and prevention advances in research. As there is currently no cure for Alzheimer's disease and other neurodegenerative diseases, many are seeking non-pharmacological treatment options in attempts to offset the disease-related cognitive and functional declines. On the basis of a growing body of research suggesting that meditation is effective in increasing grey matter volume in healthy participants, this paper systematically reviewed the literature regarding the effects of meditation on restoring grey matter volume in healthy individuals and those affected by neurodegeneration. This review searched PubMed, CINAHL, and APA PsycNET to identify original studies that included MRI imaging to measure grey matter volume in meditators and post-mindfulness-based intervention participants compared to controls. Thirteen studies were considered eligible for review and involved a wide variety of meditation techniques and included participants with and without cognitive impairment. All studies reported significant increases in grey matter volume in the meditators/intervention group, albeit in assorted regions of the brain. Limited research exists on the mechanisms through which meditation affects disease-related neurodegeneration, but preliminary evidence suggests that it may offset grey matter atrophy.

PURPOSE:To systematically evaluate and quantify the effects of Tai Chi/Qigong (TCQ) on motor (UPDRS III, balance, falls, Timed-Up-and-Go, and 6-Minute Walk) and non-motor (depression and cognition) function, and quality of life (QOL) in patients with Parkinson's disease (PD).

METHODS:A systematic search in 7 electronic databases targeted clinical studies evaluating TCQ for individuals with PD published through August 2016. Meta-analysis was used to estimate effect sizes (Hedges's g) and publication bias for randomized controlled trials (RCTs). Methodological bias in RCTs was assessed by two raters.

RESULTS:Our search identified 21 studies, 15 of which were RCTs with a total of 735 subjects. For RCTs, comparison groups included no treatment (n = 7, 47%) and active interventions (n = 8, 53%). Duration of TCQ ranged from 2 to 6 months. Methodological bias was low in 6 studies, moderate in 7, and high in 2. Fixed-effect models showed that TCQ was associated with significant improvement on most motor outcomes (UPDRS III [ES = -0.444, p < 0.001], balance [ES = 0.544, p < 0.001], Timed-Up-and-Go [ES = -0.341, p = 0.005], 6 MW [ES = -0.293, p = 0.06], falls [ES = -0.403, p = 0.004], as well as depression [ES = -0.457, p = 0.008] and QOL [ES = -0.393, p < 0.001], but not cognition [ES = -0.225, p = 0.477]). I(2) indicated limited heterogeneity. Funnel plots suggested some degree of publication bias.

CONCLUSION:Evidence to date supports a potential benefit of TCQ for improving motor function, depression and QOL for individuals with PD, and validates the need for additional large-scale trials.

UNLABELLED:In an increasingly ageing population, the incidence of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Huntington's disease are rising. While the aetiologies of these disorders are different, a number of common mechanisms that underlie their neurodegenerative components have been elucidated; namely neuroinflammation, excitotoxicity, mitochondrial dysfunction and reduced trophic support. Current therapies focus on treatment of the symptoms and attempt to delay the progression of these diseases but there is currently no cure. Modulation of the endogenous cannabinoid system is emerging as a potentially viable option in the treatment of neurodegeneration. Endocannabinoid signalling has been found to be altered in many neurodegenerative disorders. To this end, pharmacological manipulation of the endogenous cannabinoid system, as well as application of phytocannabinoids and synthetic cannabinoids have been investigated. Signalling from the CB1 and CB2 receptors are known to be involved in the regulation of Ca(2+) homeostasis, mitochondrial function, trophic support and inflammatory status, respectively, while other receptors gated by cannabinoids such as PPARγ, are gaining interest in their anti-inflammatory properties. Through multiple lines of evidence, this evolutionarily conserved neurosignalling system has shown neuroprotective capabilities and is therefore a potential target for neurodegenerative disorders. This review details the mechanisms of neurodegeneration and highlights the beneficial effects of cannabinoid treatment.

LINKED ARTICLES:This article is part of a themed section on Cannabinoids 2013. To view the other articles in this section visit undefined

Cannabidiol (CBD) is a non-psychoactive constituent of Cannabis sativa with potential to treat neurodegenerative diseases. Its neuroprotection has been mainly associated with anti-inflammatory and antioxidant events; however, other mechanisms might be involved. We investigated the involvement of neuritogenesis, NGF receptors (trkA), NGF, and neuronal proteins in the mechanism of neuroprotection of CBD against MPP(+) toxicity in PC12 cells. CBD increased cell viability, differentiation, and the expression of axonal (GAP-43) and synaptic (synaptophysin and synapsin I) proteins. Its neuritogenic effect was not dependent or additive to NGF, but it was inhibited by K252a (trkA inhibitor). CBD did not increase the expression of NGF, but protected against its decrease induced by MPP(+), probably by an indirect mechanism. We also evaluated the neuritogenesis in SH-SY5Y cells, which do not express trkA receptors. CBD did not induce neuritogenesis in this cellular model, which supports the involvement of trkA receptors. This is the first study to report the involvement of neuronal proteins and trkA in the neuroprotection of CBD. Our findings suggest that CBD has a neurorestorative potential independent of NGF that might contribute to its neuroprotection against MPP(+), a neurotoxin relevant to Parkinson's disease.