The prevalence of sarcopenia (reduced skeletal muscle strength and mass), Parkinson's disease (PD) and Parkinson's related disorders (PRD) all increase with age. They also share risk factors and pathogenetic features. An increased prevalence of sarcopenia in PD and PRD than the general population was thus postulated.Four databases were searched using predefined literature search strategies. Studies conducted in participants with PD or PRD reporting the prevalence of sarcopenia and those providing data to compute the prevalence were included. Pre-sarcopenia, probable/possible sarcopenia and confirmed sarcopenia were defined according to the main sarcopenia working groups. Risk of bias was assessed using the AXIS tool.1978 studies were identified; 97 assessed in full; 14 met inclusion criteria. The median study quality score was 15/20. The range of probable sarcopenia was 23.9 to 66.7%, and it did not change after excluding PRD participants. The prevalence of confirmed sarcopenia in participants with any parkinsonian disorder ranged from 2 to 31.4%. Including just PD participants, the range was 10.9 to 31.4%. In studies with controls, sarcopenia was more prevalent in PD and PRD. There was a positive non-significant trend between severity of motor symptoms and prevalence of sarcopenia or components of sarcopenia. High heterogeneity precluded meta-analysis, therefore there was insufficient evidence to conclude whether sarcopenia is more prevalent in PD or PRD.Probable and confirmed sarcopenia are common in PD and PRD and they may be associated with disease severity. This co-occurrence supports the value of screening for sarcopenia in parkinsonian populations.© 2023. The Author(s).

In this study, the aim was to identify the incidence of sarcopenia and dynapenia according to disease stage among idiopathic Parkinson's disease (IPD) patients and collect data to illuminate precautions related to reducing the disease load.The study was completed with 166 patients divided by stage according to modified Hoehn and Yahr (HYR) criteria and 249 healthy volunteers aged from 18 to 39 and 68 to 75 years met the inclusion criteria. In our prospective and cross-sectional study, patients with IPD according to "UK Brain Bank" diagnostic criteria had the Unified Parkinson's Disease Rating Scale (UPDRS) and HYR scales applied. The patient and control groups had skeletal muscle mass index (SMMI), muscle power, and physical performance assessed. Diagnosis of sarcopenia used the European Working Group on Sarcopenia in Older People (EWGSOP) diagnostic criteria.In our study, in parallel with the increase in disease stage among IPD patients, the incidence of sarcopenia (led by severe sarcopenia) and dynapenia was high compared to that among the control group of the same age.In the early stages of chronic progressive diseases like IPD, identification of sarcopenia and dynapenia is important considering the limitations of disease-preventive effects in treatments applied after diagnosis.

Background: Parkinson's disease (PD) and sarcopenia are two common diseases in aging people. To date, the prevalence of sarcopenia in PD patients and the relationship between clinical features and sarcopenia in PD patients are not clear. The aim of the study was to (1) assess the prevalence of sarcopenia in PD patients and (2) reveal the clinical features between PD patients with and without sarcopenia.

Sarcopenia and frailty are found in up to one-third of the general elderly population. Both are associated with major adverse health outcomes such as nursing home placement, disability, decreased quality of life, and death. Data on the frequency of both syndromes in Parkinson's disease (PD), however, are very limited.We aimed to screen for sarcopenia and frailty in PD patients and to assess potential associations of both geriatric syndromes with demographic and clinical parameters as well as quality of life.In this observational, cross-sectional study, we included 104 PD patients from a tertiary center and 330 non-PD controls from a population-based cohort aged > 65 years. All groups were screened for sarcopenia using the SARC-F score and for frailty using the Clinical Frailty Scale of the Canadian Study of Health and Aging (CSHA CFS). Prevalence rates of sarcopenia and frailty were also assessed in 18 PD patients from a population-based cohort aged > 65 years. Moreover, PD patients from the tertiary center were evaluated for motor and non-motor symptoms, quality of life, and dependency.The prevalence of sarcopenia was 55.8% (95% CI: 46.2-64.9%) in PD patients from the tertiary center and 8.2% (5.7-11.7%; p < 0.001) in non-PD controls. Frailty was detected in 35.6% (27.0-45.2%) and 5.2% (3.2-8.1%; p < 0.001). Prevalence rates for sarcopenia and frailty were 33.3% (16.1-56.4%; p = 0.004) and 22.2% (8.5-45.8%; p = 0.017) in the community-based PD sample. Both sarcopenia and frailty were significantly associated with longer disease duration, higher motor impairment, higher Hoehn and Yahr stages, decreased quality of life, higher frequency of falls, a higher non-motor symptom burden, institutionalization, and higher care levels in PD patients from a tertiary center compared to not affected PD patients (all p < 0.05).Both frailty and sarcopenia are more common in PD patients than in the general community and are associated with a more adverse course of the disease. Future studies should look into underlying risk factors for the occurrence of sarcopenia and frailty in PD patients and into adequate management to prevent and mitigate them.© 2018 S. Karger AG, Basel.

Frailty is a common negative consequence of ageing. Sarcopenia, the syndrome of loss of muscle mass, quality and strength, is more common in older adults and has been considered a precursor syndrome or the physical manifestation of frailty. The pathophysiology of both syndromes is incompletely described with multiple causes, inter-relationships and complex pathways proposed. Age-associated changes to the immune system (both immunesenescence, the decline in immune function with ageing, and inflammageing, a state of chronic inflammation) have been suggested as contributors to sarcopenia and frailty but a direct causative role remains to be established. Frailty, sarcopenia and immunesenescence are commonly described in older adults but are not ubiquitous to ageing. There is evidence that all three conditions are reversible and all three appear to share common inflammatory drivers. It is unclear whether frailty, sarcopenia and immunesenescence are separate entities that co-occur due to coincidental or potentially confounding factors, or whether they are more intimately linked by the same underlying cellular mechanisms. This review explores these possibilities focusing on innate immunity, and in particular associations with neutrophil dysfunction, inflammation and known mechanisms described to date. Furthermore, we consider whether the age-related decline in immune cell function (such as neutrophil migration), increased inflammation and the dysregulation of the phosphoinositide 3-kinase (PI3K)-Akt pathway in neutrophils could contribute pathogenically to sarcopenia and frailty.Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.

Adult skeletal tissue is composed of heterogeneous population of cells that constantly self-renew by means of a controlled process of activation and proliferation of tissue-resident stem cells named satellite cells. Many growth factors, cytokines and myokines produced by skeletal muscle cells play critical roles in local regulation of the inflammatory process and skeletal muscle regeneration during different pathological conditions. IL-6 is a pleiotropic cytokine released in large amount during infection, autoimmunity and cancer. Low levels of IL-6 can promote activation of satellite cells and myotube regeneration while chronically elevated production promote skeletal muscle wasting. These distinct effects may be explained by a crosstalk of the IL-6/IL-6 receptor and gp130 trans-signaling pathway that oppose to regenerative and anti-inflammatory of the classical IL-6 receptor signaling pathway. Here we discuss on potential therapeutic strategies using monoclonal antibodies to IL-6R for the treatment of skeletal muscle wasting and cachexia. We also highlight on the IL-6/JAK/STAT and FGF/p38 alpha beta MAPK signaling pathways in satellite cell activation and the use of protein kinase inhibitors for tailoring and optimizing satellite cell proliferation during the skeletal muscle renewal. Future investigations on the roles of the IL-6 classical and trans-signaling pathways in both immune and non-immune cells in skeletal muscle tissue will provide new basis for therapeutic approaches to reverse atrophy and degeneration of skeletal muscles in cancer and inflammatory diseases.

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Some of the inherited forms of the disease are caused by mutations in the alpha-synuclein gene and the triplication of its locus. Oxidative stress has been proposed as a central mechanism for the progression of the disease although its relation with alpha-synuclein toxicity remains obscure. Targeted expression of human alpha-synuclein has been effectively used to recreate the pathology of PD in Drosophila melanogaster and it has been proved an excellent tool for the study of testable hypothesis in relation to the disease. We show that dopaminergic neurons are specifically sensitive to hyperoxia induced oxidative stress and that mutant forms of alpha-synuclein show an enhanced toxicity under these conditions suggesting synergic interactions. In addition, the co-expression of Cu/Zn superoxid dismutase protects against the dopaminergic neuronal loss induced by mutant alpha-synuclein overexpression thus identifying oxidative stress as an important causative factor in the pathology of autosomal-dominant Parkinsonism.

This article provides an overview of the clinical presentation, investigations, and treatment options for gastrointestinal tract (GIT) dysfunction in patients with Parkinson's disease (PD) and other movement disorders.GIT dysfunction commonly appears as constipation and fecal incontinence (mostly overflow, accompanied with sphincter failure in multiple system atrophy [MSA]). Bowel dysfunction (underactive) occurs irrespectively from the site of the neurologic lesion, which is in contrast to site-dependent bladder dysfunction (brain, overactive; periphery, underactive). GI emergencies may arise, including intestinal pseudo-obstruction, intussusception, volvulus, and stercoral ulcer (ulcer of the colon due to pressure and irritation resulting from severe, prolonged constipation). Bowel function tests in neurologic patients often show a combination of slow transit and anorectal dysfunction. Management for slow transit constipation includes bulking agents, softening agents, yogurt/probiotics, and prokinetic agents. Suppositories, botulinum toxin injections, and transanal irrigation are options for managing anorectal constipation.Function of the bowel is commonly affected in PD and other movement disorders. Neurologists play an important role in assessing bowel symptoms in their patients and planning treatment strategies, often in collaboration with specialist teams.

Research on eating behaviours has extensively highlighted that cognitive systems interact with the metabolic system in driving food intake and in influencing body weight regulation. Parkinson's disease is a good model for studying these complex interactions since alterations in both body weight and cognitive domains have been frequently reported among these patients. Interestingly, even if different non-motor symptoms may characterize the course of the disease, their contribution to weight and food preference has been poorly investigated. This review describes body weight alterations and eating habits in patients with Parkinson's disease, including those who underwent deep brain stimulation surgery. In particular, the review considers the link between non-motor symptoms, affecting sensory perception, cognition, mood and motivation, and food intake and weight alterations. The take home message is twofold. First, we recommend a comprehensive approach in order to develop effective strategies in the management of patients' weight. Second, we also suggest that investigating this issue in patients with Parkinson's disease may provide some useful information about the mechanisms underlying food and weight regulation in healthy subjects. Copyright © 2014 Elsevier Ltd. All rights reserved.

Background: Non-motor symptoms in Parkinson’s disease (PD) are often associated with a negative impact on the patients’ quality of life and on their weight regulation. The aim of this study was to assess the effect of olfactory and gustatory dysfunction, apathy, fatigue, depression, and motor symptoms on weight regulation in PD patients. Methods: We analyzed 112 participants, 63 PD patients (mean age ± SD: 69.2 ± 10.1), and 49 controls (mean age ± SD: 68 ± 9.6). For each participant we collected age, weight, height, BMI, olfactory and gustatory function, cognitive performance, apathy and fatigue. Results: Our data showed that 61.9% (n = 39) of PD patients had hyposmia, while 38.1% (n = 24) had anosmia. In PD patients, we observed a significant effect of Unified Parkinson’s Disease Rating Scale (UPDRS), apathy, odor threshold, sweet perception and fatigue on weight regulation. Instead, there was no significant effect for depression and levodopa equivalent daily dosage (LEDD). Conclusion: Our results suggest that PD non-motor symptoms such as olfactory/gustatory deficits and mood disorders may influence body weight.

The substantial weight loss in Parkinson's patients may be related to direct influences of levodopa treatment on fat mobilization/oxidation. We assessed systemic and local metabolic responses to levodopa/benserazide in patients with idiopathic Parkinson's disease.We studied 10 Parkinson's disease patients and examined adipose tissue and skeletal muscle metabolism directly with microdialysis. We monitored dialysate concentrations of ethanol, glucose, lactate, pyruvate, and glycerol to assess tissue blood flow and metabolism before and after levodopa/benserazide intake. We also conducted in vitro studies on adipocytes from healthy women.Levodopa/benserazide increased serum levodopa, 3,4-dihydroxyphenylacetic acid (DOPAC), and norepinephrine (P < 0.01). Serum adipose tissue and skeletal muscle glycerol did not change or decreased. Adipose tissue glycerol was inversely correlated with serum levodopa concentrations (P < 0.05). In isolated adipocytes, levodopa attenuated isoproterenol-induced glycerol release (P < 0.05).Levodopa/benserazide elicits pronounced metabolic changes in both adipose tissue and skeletal muscle with a switch from lipid to carbohydrate metabolism. In adipose tissue, levodopa/benserazide failed to activate lipolysis. Therefore, we suggest that levodopa/benserazide does not induce fat wasting through direct and acute influences on adipose tissue metabolism.

The exact mechanism of Parkinson's disease (PD) is not fully understood yet, but it is suggested that inflammation is one of its contributing factors. Among several inflammatory factors, adipokines, especially leptin may have a great role in this mechanism; since it is not only causing inflammation, but it can also play other roles in the body that may contribute to the symptoms described for PD. Regarding the contradictions in the association of serum leptin levels with Parkinson's disease, a systematic review and meta-analysis was performed to have a more accurate estimation of this relationship.Published literature was obtained by searching PubMed, Embase, Cochrane Library, Scopus, Ovid, ProQuest and Google Scholar. Random-effect model analysis was used to calculate pooled standard mean difference (SMD) with 95% confidence interval (CI). Heterogeneity was tested with the heterogeneity statistic Q and quantified using I. Newcastle-Ottawa scale was used to assess the study quality.Six studies including a total number of 198 PD patients and 182 controls were finally included in the meta-analysis. Serum leptin levels in PD patients were non-significantly lower than those in control group (SMD = -0.40 ng/ml, 95% CI -2.33-1.53). Subgroup analyses revealed that serum leptin levels of PD patients and controls in either females or males didn't show any significant difference.This meta-analysis revealed that leptin level doesn't show any significant difference between PD patients and healthy controls, even when taking the participants' gender into consideration.Copyright © 2020 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.

Sarcopenia is an age‐related condition characterized by a progressive and systemic decline in skeletal muscle mass, quality, and strength. The incidence of sarcopenia contains sex‐specific aspects, indicating the contribution of sex hormones to its pathophysiology. This review focuses on changing trends in sarcopenia, discusses alterations in definitions and diagnostic criteria, and emphasizes the association between sarcopenia and sex hormones.

Maintenance of skeletal muscle mass throughout the life course is key for the regulation of health, with physical activity a critical component of this, in part, due to its influence upon key hormones such as testosterone, estrogen, growth hormone (GH), and insulin-like growth factor (IGF). Despite the importance of these hormones for the regulation of skeletal muscle mass in response to different types of exercise, their interaction with the processes controlling muscle mass remain unclear. This review presents evidence on the importance of these hormones in the regulation of skeletal muscle mass and their responses, and involvement in muscle adaptation to resistance exercise. Highlighting the key role testosterone plays as a primary anabolic hormone in muscle adaptation following exercise training, through its interaction with anabolic signaling pathways and other hormones via the androgen receptor (AR), this review also describes the potential importance of fluctuations in other hormones such as GH and IGF-1 in concert with dietary amino acid availability; and the role of estrogen, under the influence of the menstrual cycle and menopause, being especially important in adaptive exercise responses in women. Finally, the downstream mechanisms by which these hormones impact regulation of muscle protein turnover (synthesis and breakdown), and thus muscle mass are discussed. Advances in our understanding of hormones that impact protein turnover throughout life offers great relevance, not just for athletes, but also for the general and clinical populations alike.

Vitamin D deficiency is a common health problem worldwide, in particular among older people. Vitamin D regulates and modulates the physiology and function of multiple human systems, including the skeletal muscle. The effect of vitamin D on the muscle has been widely investigated, suggesting that this hormone can stimulate the proliferation and differentiation of skeletal muscle fibers, maintaining and improving muscle strength and physical performance. Older persons have a higher prevalence of low Vitamin D levels as a consequence of low dietary intake and reduced ultraviolet irradiation of the skin. Therefore, older people with vitamin D deficiency might be at risk of sarcopenia, a geriatric syndrome characterized by the progressive loss of skeletal muscle mass and strength often complicated by adverse events, such as falls, disability hospitalization and death. Several randomized clinical trials have been conducted to investigate the effect of oral vitamin D supplementation in older patients to prevent or treat sarcopenia, but results are still controversial. In this narrative review we summarize the biological, clinical and epidemiological evidence supporting the hypothesis of a causal association between Vitamin D deficiency and an increased risk of sarcopenia in older people.

Parkinson's disease (PD) involves the loss of dopamine neurons and accumulation of alpha-synuclein (α-syn), leading to Lewy bodies. While α-syn-targeting immunotherapies show promise, clinical application is challenging. Emerging strategies include nano-platforms for targeted delivery and imaging, and cell-based therapies with patient-specific dopaminergic neurons, aiming to enhance treatment effectiveness despite challenges. Exosome-based methodologies are emerging as a promising area of research in PD due to their role in the spread of α-syn pathology. Exosomes are small extracellular vesicles that can carry misfolded α-syn and transfer it between cells, contributing to the progression of PD. They can be isolated from biological fluids such as blood and cerebrospinal fluid, making them valuable biomarkers for the disease. Additionally, engineering exosomes to deliver therapeutic agents, including small molecules, RNA, or proteins, offers a novel approach for targeted therapy, capitalizing on their natural ability to cross the blood-brain barrier (BBB). Ongoing studies are evaluating the safety and efficacy of these engineered exosomes in clinical settings. This review explores the role of exosomes in PD, focusing on their potential for diagnosis, treatment, and understanding of pathology. It highlights advancements and future directions in using exosomes as biomarkers and therapeutic tools.© 2025. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

What is the central question of this study? Capillary rarefaction is found in diabetic and aged muscle, whereas exercise increases skeletal muscle angiogenesis. The association implies a crosstalk between muscle cells and endothelial cells. The underlying mechanisms mediating the crosstalk between these cells remains to be elucidated fully. What is the main finding and its importance? Endothelial cell functions are regulated by skeletal muscle cell-derived exosomes via a vascular endothelial growth factor-independent pathway. This study reveals a new mechanism mediating the crosstalk between skeletal muscle cells and endothelial cells.Loss of skeletal muscle capillarization, known as capillary rarefaction, is found in type 2 diabetes, chronic heart failure and healthy ageing and is associated with impaired delivery of substrates to the muscle. However, the interaction and communication of skeletal muscle with endothelial cells in the regulation of capillaries surrounding the muscle remains elusive. Exosomes are a type of secreted extracellular vesicle containing mRNAs, proteins and, especially, microRNAs that exert paracrine and endocrine effects. In this study, we investigated whether skeletal muscle-derived exosomes (SkM-Exo) regulate the endothelial cell functions of angiogenesis. We demonstrated that C2C12 myotube-derived exosomes improved endothelial cell functions, assessed by the proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs), which were increased by 20, 23 and 40%, respectively, after SkM-Exo exposure. The SkM-Exo failed to activate HUVEC vascular endothelial growth factor (VEGF) signalling. The SkM-Exo increased HUVEC reactive oxygen species and activated the nuclear factor-κB pathway, suggesting that SkM-Exo-induced angiogenesis was mediated by a VEGF-independent pathway. In addition, several angiogenic microRNAs were packaged in SkM-Exo, with miR-130a being particularly enriched and successfully transferred from SkM-Exo to HUVECs. Delivery of miRNAs into endothelial cells might explain the enhancement of reactive oxygen species production and angiogenesis by SkM-Exo. The potential angiogenic effect of SkM-Exo could provide an effective therapy for promoting skeletal muscle angiogenesis in diseases characterized by capillary rarefaction or inadequate angiogenesis.© 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.

MicroRNA (miRNA)s are a class of non-coding RNAs that regulate gene expression post-transcriptionally. Muscle-specific miRNA, miRNA (miR)-1, miR-133 and miR-206 play a crucial role in the regulation of muscle development and homeostasis. Muscle injuries are a common musculoskeletal disorder, and the most effective treatment has not been established yet. The purpose of this study was to demonstrate that a local injection of double-stranded (ds) miR-1, miR-133 and 206 can accelerate muscle regeneration in a rat skeletal muscle injury model. After the laceration of the rat tibialis anterior muscle, ds miR-1, 133 and 206 mixture mediated atelocollagen was injected into the injured site. The control group was injected with control siRNA. At 1 week after injury, an injection of miRNAs could enhance muscle regeneration morphologically and physiologically, and prevent fibrosis effectively compared to the control siRNA. Administration of exogenous miR-1, 133 and 206 can induce expression of myogenic markers, MyoD1, myogenin and Pax7 in mRNA and expression in the protein level at 3 and 7 days after injury. The combination of miR-1, 133 and 206 can promote myotube differentiation, and the expression of MyoD1, myogenin and Pax7 were up-regulated in C2C12 cells in vitro. Local injection of miR-1, 133 and 206 could be a novel therapeutic strategy in the treatment of skeletal muscle injury.© 2009 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

Background: Parkinson’s disease (PD) is a common neurodegenerative disease associated with progressive gray matter atrophy. In addition to motor function disorder, frailty and decreased muscle mass potentially contribute to increased morbidity risk. Objective: This study aimed to investigate the associations between lean muscle loss and gray matter volume (GMV) in PD patients. Methods: Thirty patients with PD and fifteen healthy controls underwent brain and bilateral thigh MRIs. The IDEAL sequence was employed, measuring the regions of interest (ROI) of fat percentage at the 50% point of femur length. Voxel-base morphometry (VBM) was used to assess regional gray matter volume differences between groups. Further correlation analysis was performed to evaluate the changes between gray matter volume and fatty percentage of the bilateral thigh after adjusting for age and gender. Multiple linear regression analysis was applied to evaluate the risk factor of core muscle loss in PD patients. Results: Compared with controls, patients with PD had significantly higher thigh fat percentage and smaller gray matter volume of several brain locations of the default mode network (DMN), specifically the left superior temporal gyrus, right uncus, and left inferior temporal gyrus, revealing association with higher thigh fat percentage. Further multiple linear regression analysis indicated that higher thigh fat percentage is associated with gender (female), increased disease duration, and smaller gray matter volume of the left superior temporal gyrus and right uncus in PD patients. Conclusions: Patients with PD experience core muscle loss in the thigh, associated with default mode network (DMN) degeneration, longer disease duration, and female gender. Identification of risk factors associated with lean muscle mass loss may assist in early prevention of comorbidities such as sarcopenia.

Background: Sarcopenia is critically associated with morbidity and mortality in the progression of Parkinson’s disease (PD). However, analyses of clinical severity and brain changes, such as white matter (WM) alterations in PD patients with sarcopenia are limited. Further understanding of the factors associated with sarcopenia may provide a focused screen and potential for early intervention in PD patients. Methods: 52 PD patients and 19 healthy participants accepted dual-energy X-ray absorptiometry to measure the body composition. Using diffusion tensor imaging, the difference of WM integrity was measured between PD patients with sarcopenia (PDSa) and without sarcopenia (PDNSa). Multivariate analysis was performed to explore the relationships between clinical factors, WM integrity, and sarcopenia in PD patients. Results: 21 PD patients (40.4%) had sarcopenia. PDSa had a higher Unified Parkinson’s Disease Rating Scale (UPDRS III) score, lower body mass index (BMI) and lower fat weight compared with the PDNSa. Additionally, PDSa patients exhibited lower fractional anisotropy accompanied by higher radial diffusivity and/or higher mean diffusivity in the fronto-striato-thalamic circuits, including bilateral cingulum, left superior longitudinal fasciculus, left genu of corpus callosum, and right anterior thalamic radiation, which participate in the executive function. In addition, decreased muscle mass was associated with worse WM integrity in these regions. Multiple linear regression analysis revealed that WM integrity in the left cingulum, right anterior thalamic radiation, together with gender (male) significantly predicted muscle mass in PD patients. Conclusions: WM alterations in the executive network, such as the fronto-striato-thalamic circuits, may indicate a risk factor for ongoing sarcopenia in PD patients. The effectiveness of using executive function to serve as a prodromal marker of sarcopenia in PD patients should be evaluated in future studies.

<b><i>Introduction:</i></b> Pathogenesis in a subgroup of sarcopenic patients seems to be based on a reduced number of motor neurons. This study aimed at investigating the overlap between sarcopenia and neurodegeneration, as reflected by a low number of motor neurons in patients with Parkinsonian syndromes (PS). <b><i>Methods:</i></b> The motor unit number index (MUNIX) of the hypothenar muscle was used to assess the number and size (MUSIX) of motor units (MUs) in patients with idiopathic Parkinson disease (iPD, <i>n</i> = 53), patients with atypical Parkinsonian syndrome (aPS, <i>n</i> = 21), and a control group (<i>n</i> = 30). Mean age of participants was 70.3 years and 54.1% were female. Skeletal muscle mass by bioelectrical impedance analysis, hand-grip strength and gait speed were measured. Based on these assessments, sarcopenia was diagnosed according to the criteria of the European Working Group on Sarcopenia in Older People.<b><i> Results:</i></b> Sarcopenia criteria were met by 10 patients with PS (13.5%). The study group had significantly lower MUNIX values than the control group (109 [SD ±39.1] vs. 129 [SD ±45.1]; <i>p</i> = 0.020) even after adjustment for age and sex. Three of the 5 sarcopenic iPD patients (75%) had pathological low MUNIX values (&#x3c;80). <b><i>Discussion/Conclusion:</i></b> Sarcopenia is a frequent comorbidity in PS. The pathologically low MUNIX values found in 75% of our sarcopenic iPD patients provides further support for the existence of a neurodegenerative overlap syndrome with a reduced number of MUs potentially leading to sarcopenia. This finding warrants further evaluation.

The escalation of life expectancy is accompanied by an increase in the prevalence of age-related conditions, such as sarcopenia. Sarcopenia, a muscle condition defined by low muscle strength, muscle quality or quantity, and physical performance, has a high prevalence among the elderly and is associated to increased mortality. The neuromuscular system has been emerging as a key contributor to sarcopenia pathogenesis. Indeed, the age-related degeneration of the neuromuscular junction (NMJ) function and structure may contribute to the loss of muscle strength and ultimately to the loss of muscle mass that characterize sarcopenia. The present mini-review discusses important signaling pathways involved in the function and maintenance of the NMJ, giving emphasis to the ones that might contribute to sarcopenia pathogenesis. Some conceivable biomarkers, such as C-terminal agrin fragment (CAF) and brain-derived neurotrophic factor (BDNF), and therapeutic targets, namely acetylcholine and calcitonin gene-related peptide (CGRP), can be retrieved, making way to future studies to validate their clinical use.© 2021. The Author(s), under exclusive licence to American Aging Association.

The European Working Group on Sarcopenia in Older People (EWGSOP) developed a practical clinical definition and consensus diagnostic criteria for age-related sarcopenia. EWGSOP included representatives from four participant organisations, i.e. the European Geriatric Medicine Society, the European Society for Clinical Nutrition and Metabolism, the International Association of Gerontology and Geriatrics-European Region and the International Association of Nutrition and Aging. These organisations endorsed the findings in the final document. The group met and addressed the following questions, using the medical literature to build evidence-based answers: (i) What is sarcopenia? (ii) What parameters define sarcopenia? (iii) What variables reflect these parameters, and what measurement tools and cut-off points can be used? (iv) How does sarcopenia relate to cachexia, frailty and sarcopenic obesity? For the diagnosis of sarcopenia, EWGSOP recommends using the presence of both low muscle mass + low muscle function (strength or performance). EWGSOP variously applies these characteristics to further define conceptual stages as 'presarcopenia', 'sarcopenia' and 'severe sarcopenia'. EWGSOP reviewed a wide range of tools that can be used to measure the specific variables of muscle mass, muscle strength and physical performance. Our paper summarises currently available data defining sarcopenia cut-off points by age and gender; suggests an algorithm for sarcopenia case finding in older individuals based on measurements of gait speed, grip strength and muscle mass; and presents a list of suggested primary and secondary outcome domains for research. Once an operational definition of sarcopenia is adopted and included in the mainstream of comprehensive geriatric assessment, the next steps are to define the natural course of sarcopenia and to develop and define effective treatment.

Sarcopenia, the age-associated loss of skeletal muscle mass and function, has considerable societal consequences for the development of frailty, disability, and health care planning. A group of geriatricians and scientists from academia and industry met in Rome, Italy, on November 18, 2009, to arrive at a consensus definition of sarcopenia. The current consensus definition was approved unanimously by the meeting participants and is as follows: Sarcopenia is defined as the age-associated loss of skeletal muscle mass and function. The causes of sarcopenia are multifactorial and can include disuse, altered endocrine function, chronic diseases, inflammation, insulin resistance, and nutritional deficiencies. Although cachexia may be a component of sarcopenia, the 2 conditions are not the same. The diagnosis of sarcopenia should be considered in all older patients who present with observed declines in physical function, strength, or overall health. Sarcopenia should specifically be considered in patients who are bedridden, cannot independently rise from a chair, or who have a measured gait speed less that 1 m/s(-1). Patients who meet these criteria should further undergo body composition assessment using dual energy x-ray absorptiometry with sarcopenia being defined using currently validated definitions. A diagnosis of sarcopenia is consistent with a gait speed of less than 1 m·s(-1) and an objectively measured low muscle mass (eg, appendicular mass relative to ht(2) that is ≤ 7.23 kg/m(2) in men and ≤ 5.67 kg/m(2) in women). Sarcopenia is a highly prevalent condition in older persons that leads to disability, hospitalization, and death.Copyright © 2011 American Medical Directors Association. Published by Elsevier Inc. All rights reserved.

Sarcopenia, defined as an age-associated loss of skeletal muscle function and muscle mass, occurs in approximately 6 - 22 % of older adults. This paper presents evidence-based clinical practice guidelines for screening, diagnosis and management of sarcopenia from the task force of the International Conference on Sarcopenia and Frailty Research (ICSFR).To develop the guidelines, we drew upon the best available evidence from two systematic reviews paired with consensus statements by international working groups on sarcopenia. Eight topics were selected for the recommendations: (i) defining sarcopenia; (ii) screening and diagnosis; (iii) physical activity prescription; (iv) protein supplementation; (v) vitamin D supplementation; (vi) anabolic hormone prescription; (vii) medications under development; and (viii) research. The ICSFR task force evaluated the evidence behind each topic including the quality of evidence, the benefit-harm balance of treatment, patient preferences/values, and cost-effectiveness. Recommendations were graded as either strong or conditional (weak) as per the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Consensus was achieved via one face-to-face workshop and a modified Delphi process.We make a conditional recommendation for the use of an internationally accepted measurement tool for the diagnosis of sarcopenia including the EWGSOP and FNIH definitions, and advocate for rapid screening using gait speed or the SARC-F. To treat sarcopenia, we strongly recommend the prescription of resistance-based physical activity, and conditionally recommend protein supplementation/a protein-rich diet. No recommendation is given for Vitamin D supplementation or for anabolic hormone prescription. There is a lack of robust evidence to assess the strength of other treatment options.

The aim of the present systematic review and meta-analysis was to synthesize evidence associated with the functional and clinical effectiveness of rhythmic cueing, dance, or resistance training (RT) on motor and non-motor parameters in Parkinson's Disease patients, and to provide a comparative perspective not offered by existing systematic reviews.

Bradykinesia and muscle weaknesses are common symptoms of Parkinson's Disease (PD) and are associated with impaired functional performance, increased risk of falls, and reduced quality of life. Recent studies have pointed to progressive resistance training (PRT) as an effective method to control and reduce these symptoms, increasing possibilities to treat the disease. However, few studies have focused on assessing the PRT effects in the short-term. Therefore, the present study aimed to assess the short-term PRT effects on people with PD, in order to offer new parameters for a better understanding of its effects, so as an adequation and PRT use as a complementary therapy.Forty individuals diagnosed with PD from stage 1 to 3 on the Hoehn and Yahr scale took part on the study and were allocated into 2 groups; Training Group (TG) performed a 9-week RT program twice a week, and the Control Group (CG) attended disease lectures. Bradykinesia UPDRS subscale (BSS), knee extensors isokinetic strength, Ten Meters Walk Test (TMW), Timed Up&Go Test (TUG) and 30-Second Chair Stand (T30) were measured before and after the intervention period. Statistical significance was set at p ≤ 0.05.Significant time was noted by the group interaction for all functional tests (TUG, T30, and TWM; all p < 0.01) and BSS (p < 0.01). Post hoc analyses revealed that these differences were driven by significant improvements in these dependent variables (all p < 0.01) while the CG remained unchanged (all p > 0.05). Moreover, TUG, T30, TWM, and BSS were significantly different between TG and CG in the post-training assessments (all p < 0.01). Isokinetic muscle strength was slightly increased in the TG (2.4%) and decreased in the CG (-2.2%), but statistical analyses did not reach significance for interaction but only a trend (p = 0.12).The results indicate that 9 weeks of PRT reduces bradykinesia and improves functional performance in patients with mild to moderate PD. These findings reinforce this mode of exercise as an important component of public health promotion programs for PD.© 2020 Vieira de Moraes Filho et al.

Sarcopenia has been recognized as a muscle disease, with adverse consequences on health. Updated recommendations, aimed at increasing awareness of sarcopenia and its accompanying risks, have been produced to urge the early detection and treatment of this disease. Recommended treatment is based on an individually tailored resistance exercise training program, the optimization of protein intake using high-quality protein sources (i.e., whey protein) in order to provide a high amount of essential amino acids—particularly leucine—and addressing vitamin D deficiency/insufficiency. The purpose of this review is to collate and describe all of the relevant efficacy studies carried out with a muscle-targeted oral nutritional supplementation (MT-ONS)—namely a whey-protein-based, leucine- and vitamin D-enriched formula aimed at optimizing their intake and satisfying their requirements—in different patient populations and clinical settings in order to determine if there is enough evidence to recommend prescription for the treatment of sarcopenia or its prevention in high-risk patient populations. Trials using a MT-ONS with or without a concomitant physical exercise program were systematically searched (up to June 2021), and those addressing relevant endpoints (muscle mass, physical performance and function) were critically reviewed. In total, 10 articles providing efficacy data from eight trials were identified and narratively reviewed. As far as older patients with sarcopenia are concerned, MT-ONS has been pertinently tested in six clinical trials (duration 4–52 weeks), mostly using a high-quality randomized controlled trial design and demonstrating efficacy in increasing the muscle mass and strength, as well as the physical performance versus iso-caloric placebo or standard practice. Consistent results have been observed in various clinical settings (community, rehabilitation centers, care homes), with or without adjunctive physical exercise programs. A positive effect on markers of inflammation has also been shown. A muscle-protein-sparing effect, with benefits on physical performance and function, has also been demonstrated in patients at risk of losing skeletal muscle mass (three trials), such as older patients undergoing weight loss or intensive rehabilitation programs associated with neurological disability (Parkinson’s disease). MT-ONS has demonstrated not only a significant efficacy in clinical variables, but also a positive impact on healthcare resource consumption in the rehabilitation setting (length of stay and duration of rehabilitation). In summary, MT-ONS, alone or in association with an appropriate exercise program, is an effective therapy for older patients with sarcopenia and should be offered as a first-line treatment, not only to improve clinical outcomes but also to reduce healthcare resource consumption, particularly in patients admitted to a rehabilitation center.

Sulforaphane (SFN) is a phytocompound belonging to the isothiocyanate family. Although it was also found in seeds and mature plants, SFN is mainly present in sprouts of many cruciferous vegetables, including cabbage, broccoli, cauliflower, and Brussels sprouts. SFN is produced by the conversion of glucoraphanin through the enzyme myrosinase, which leads to the formation of this isothiocyanate. SFN is especially characterized by antioxidant, anti-inflammatory, and anti-apoptotic properties, and for this reason, it aroused the interest of researchers. The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.