Active clinical trials for "Parkinson Disease"

With the global ageing population, neurodegenerative disorders including synucleinopathy are major burdens to patients, carers and society. Synucleinopathy refers to a group of neurodegenerative diseases characterized by abnormal aggregation of alpha-synuclein protein in the central nervous system (CNS). Common examples of synucleinopathy are Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Among all the premotor clinical markers that have been identified, a sleep disorder known as REM sleep behavior disorder (RBD) is associated with the highest likelihood ratio of developing PD. In addition, it has been shown that almost all RBD patients (over 80%) eventually developed neurodegenerative diseases after 14 years follow-up. Gut microbiota and synucleinopathy In recent years, several key studies have advanced our understanding regarding the roles that brain-gut-microbiota axis plays in the pathogenesis of brain diseases, including PD. It has been shown that gut microbiota is implicated in a series of pathophysiological changes in PD, including motor deficits, microglia activation, and αSyn pathology in mice model with overexpression of αSyn. Furthermore, some microbiotas, such as enterobacteriaceae, have been shown to be positively associated with the severity of PD symptoms, including postural instability and gait difficulty. Limitations in previous studies and knowledge gaps Nonetheless, the answers for several key questions regarding the roles of gut microbiota in the progression of synucleinopathy are still unclear. First, whether these microbiotas found in previous studies are the causes or the effects of PD. For example, medications treating PD may also affect the gut microbiome. Moreover, the microbiota may be affected by a number of factors commonly found in PD, such as constipation per se and diet. In this regard, an influential hypothesis of synucleinopahy was proposed by Braak et al at which the early premotor features including gastro-enterology symptoms, such as constipation and RBD would predate the onset of PD by some years. Thus, it is crucial to compare the microbiota among individuals at different stages of synucleinopathy. In view of slow progression of synucleinopathy and a relatively low prevalence of synucleinopathy in the general population, it is impractical to run a prospective study to examine this research question. Finally, gut microbiota is determined by both genetic and environmental factors. A family cohort design will help to understand the genetic and environmental influences on the association between microbiota and synucleinopathy.

The purpose of this study is to provide objective measurements of abnormal movements of the body in correlation with neural activity of the brain and track how these change over time. This may allow for the development of objective evaluation of the neural activity causing abnormal movements, which may lead to the ability of the DBS system to stimulate the brain by sensing the abnormal neural activity that is causing abnormal movements.

Parkinson's disease is characterized in the advanced phases by an altered response to dopaminergic therapy for the occurrence of abnormal movements called dyskinesias, that worsens the quality of life of the patient and exposes him to comorbidities. Several data show a reduction in the amount of slow wave sleep that correlates inversely with disease duration. Since this stage of sleep is linked to mechanisms of deletion of superfluous information the investigators hypothesize that the onset of dyskinesias is related to such alteration of sleep. -This study is aimed to investigate, by means of high-density electroencephalography (hd-EEG), the sleep and in particular the slow wave in order to clarify the relations with the development of dyskinesias.

AFF008E is set-up to assess the long term effects of the 4 PD01A vaccinations that have been applied during AFF008 with regard to safety as well as immunological-, radiological and clinical activity. Accordingly, during AFF008E, no further vaccine dose will be applied. Instead, patients who were participating in AFF008 will be assessed for another 52 weeks at the occasion of 4 quarterly visits. This is offered to patients who received PD01A vaccinations but also to the patients who served as controls in AFF008. Thus, AFF008E will ensure standardized and controlled management of individuals who have received PD01A as part of AFF008, the Phase I study analyzing for the first time in humans this first in class candidate.

The cause of Parkinson's disease (PD) is currently unknown. Both environmental and genetic factors have been found to contribute to PD pathogenesis. The pathology of PD is distributed throughout the entire nervous system including the central, peripheral, and enteric nervous system. There is evidence that inflammation plays a major role in neurodegeneration in PD. In both the striatum and substantia nigra of PD patients activated microglia were found and proinflammatory cytokines (TNF, IL-1B, IL-6, iNOS) are increased in the CSF. An inflammation-driven animal model has emerged and has been widely accepted as a model of the disease based on lipopolysaccharide (LPS) induced neurotoxicity. LPS is an endotoxin found on the outer membrane of gram negative bacteria and humans are exposed to LPS through the intestinal tract. The intestinal tract and thus the enteric nervous system serve as a conduit to the central nervous system. It has been posited that the inflammatory process could gain access to the lower brainstem via the vagal nerve and then ascend through the basal mid- and forebrain until it reaches the cerebral cortex, producing various pre-motor and motor symptoms of PD along the way. LPS may be one of the inflammatory triggers involved in this process. Systemic exposure to bacterial endotoxin can be determined by measuring plasma LPS binding protein (LBP). A study of 9 patients with early PD (median Hoehn and Yahr stage 2) and age matched controls found that the PD subjects had a significantly lower mean level of plasma LBP compared to control subjects. The aim of the research plan is to establish LBP as a potential biomarker for PD across a spectrum of disease severity.

The primary objective of this study is to obtain detailed clinical information and biologic specimens from subjects with PD toward the ultimate end of identifying a biomarker of PD. Because of the inherent difficulties of using clinical outcome measures to assess disease modification, the identification of biomarkers of PD is of paramount importance. The ideal PD biomarker would be one that is easily assayed in a convenient biological sample, varies proportionally with disease severity, is abnormal during the pre-symptomatic phase of the illness, and is unaffected by drugs or other interventions used to treat PD. The existence of a sensitive biomarker with these properties would enable much more effective disease modifying research that would likely be able to take advantage of smaller and potentially shorter trials.

In a recent study it was found that neurologist care for Parkinson's provides a 20% reduction in nursing home placement, hip fracture, and death (Willis 2011). However, as the authors recognized, the investigators don't know what it is about expert care that delivers this benefit. The Parkinson's Foundation's Quality Improvement Initiative was designed to identify the components of great care that yield great outcomes. By capturing demographics, clinical interventions and outcomes over time from multiple centers across the U.S, Canada and internationally, the best care practices from different clinics and different healthcare systems will be analyzed.

Study objectives are to improve motion sensor algorithms for measuring bradykinesia in the clinic and the home, evaluate test-retest reliability of motion sensor algorithms for measuring bradykinesia compared to clinician raters, determine if participant-perceived symptom severities correlate with motion sensor measures, determine if speed, amplitude, and rhythm fluctuate differentially throughout the day in individuals with implanted deep brain stimulation systems, receive feedback on the usability of Kinesia One, and evaluate Kinesia One compliance in the home.

This study aims to evaluate the effectiveness of Rotigotine and Levodopa combination therapy for younger and older patients with Parkinson's Disease under real life conditions. Effects on ability to perform activities of daily living, sleep, medication dose and other factors will be assessed.

The purpose of this study is to evaluate whether subthalamic deep brain stimulation (STN DBS) can affect moral and economic decisions in patients with Parkinson's disease (PD).