View clinical trials related to Parkinson's Disease.
Filter by:The Harvard Biomarker Study is a Harvard-wide, longitudinal case-control study designed for discovering, replicating, and developing biomarkers for Parkinson's disease and Alzheimer's disease. High-quality biosamples and high-resolution clinical phenotypes are tracked at three visits over a two-year period for more than 2,000 individuals with early-stage PD, MCI/AD, and controls without neurologic disease. The present "Ancillary Longitudinal CSF Collection Study (short HBS2)" is an ancillary study to the parent Harvard Biomarker Study. HBS2 is funded by the NINDS. In HBS2, 75 participants are more intensely studied and followed over a three-year time period. Clinical data and blood biospecimens are collected every six months and four annual CSF collections are performed. Biospecimens and clinical data are deposited into the NINDS PD Biomarkers Program (PDBP) Repository and the Data Management Resource (DMR) and are accessible through the PDBP DMR website.
The objective of the study is to assess the effect of motor, non-motor and genetic factors on the progression of Parkinson's disease as well as its impact on complications rates. A large sample of Mexican subjects with Parkinson's disease attending several referral centers will be included. Data collected will include disease severity and motor scales, non-motor scales as well as genotyping for monogenic forms of the disease. Assessments will be performed every 6 months for two years.
Parkinson's disease patients may have severe non-motor symptoms. A common and troublesome non-motor symptom is pain. Currently these symptoms are treated with medication with limited success. Our study aims to determine whether relaxation guided imagery can alleviate pain in Parkinson's disease patients.
This proposal seeks to 1) determine whether there are biomarkers associated with Parkinson's disease (PD) susceptibility and/or progression in exosome-proteomes derived from PD patients versus controls, and 2) to determine if LRRK2 expression and/or phosphorylation are significantly lowered in the exosomes of individuals treated with the potent LRRK2 kinase inhibitor sunitinib (a multi-kinase inhibitor compound), to establish an assay for on-target effects for future LRRK2 inhibitor clinical trials.
Rationale: Visual hallucinations (VH) are the most common non-motor symptoms in Parkinson's disease (PD). As an independent predictor for cognitive decline and nursing home placement they form an important disability milestone in the course of PD. According to current clinical guidelines minor VH do not require treatment per se. But as minor VH precede the stage of major VH without insight and PD associated psychosis (PDP) they offer an opportunity for early intervention. Neuroleptic drugs delay the transition into PDP but are unsuitable for early treatment of VH due to their side effects. We hypothesize that cholinesterase inhibitors (ChEI) are a well-tolerated alternative for the early treatment of minor VH to delay the progression to PDP, and that brain network analysis is suitable to predict treatment response. Objective: Investigate whether early treatment with ChEI delays the progression of minor VH to major VH without insight or PDP. In addition, we will measure motor control, psychotic symptoms, cognitive impairment, mood disorders, daytime sleepiness, adverse events and compliance, disability, caregiver burden and care use. We assess the cost-effectiveness of early chronic treatment of VH with ChEI. Finally, we analyse changes of functional brain networks before and during treatment. Study design: A randomized, double blind, placebo-controlled, multi-center trial with an economic evaluation. Study population: 168 patients with PD and VH after fulfilling the in-and exclusion criteria. Intervention: Rivastigmine capsule 6 mg BID or placebo BID for 24 months. Main study parameters/endpoints: The primary outcome measure is the median time until PD patients with minor VH progress to major VH without insight. The clinical endpoint is defined as the start with antipsychotic treatment. Secondary outcome measures are changes in motor control, psychotic symptoms, cognitive impairment, mood disorders, daytime sleepiness, cholinergic deficiency, the number of adverse events, compliance, disability and caregiver burden. The median time until PD patients with minor VH progress to PD dementia is measured by means of changes in cognitive function. The secondary neurophysiological outcome measures are peak frequency, functional connectivity, topological network organisation and the direction of information flow. All relevant costs will be measured and valued. Nature and extent of the burden and risks associated with participation, benefit and group relatedness: The burden of participation consists of a total of 5 clinical visits (every 6 months), 5 telephone interviews on adverse events during the escalation phase and 9 questionnaires on health related costs (every 3 months). In a subgroup 3 additional visits for EEG recording are needed. There is a risk for adverse reactions with rivastigmine treatment; the most common are nausea and vomiting.
The study is designed to assess the long term tolerability of ProSavin and whether it is safe and efficacious in patients administered ProSavin from the PS1/001/07 study .
Persons with Morbus Parkinson commonly develop gait and balance disorders leading to dependence, loss of mobility and a high risk of falling. This study investigates the effectiveness of a sensorimotor treadmill intervention to improve walking and balance abilities in persons with early stages of Parkinson's disease. The sensorimotor treadmill training is conducted on a special treadmill device which is challenging the participants by small oscillations. This intervention, which is supposed to simulate walking on natural, uneven surfaces, is compared to a conventional treadmill training. Hypothesis: Sensorimotor treadmill training leads to larger improvements in walking and balance abilities as compared to conventional treadmill exercise.
GM608 is an endogenous human embryonic stage neural regulatory and signaling peptide that controls the development, monitoring and correction of the human nervous system. The study drug is an oligopeptide with a sequence identical to one of the active sites of human Motoneuronotrophic Factor and is manufactured by solid phase synthesis. Preclinical research indicates it to be a neuro-protective agent in animal models of PD, other neuro-degenerative diseases and stroke. This trial is designed to test proof of principle, i.e. determine if a 2-week treatment with this agent can restore the non-functioning nigral dopaminergic neurons in PD over a 3 month period, during which the placebo-treated arm is expected to have little or no worsening of the total UPDRS (Unified Parkinson's Disease Rating Scale)score compared to baseline. Study Objectives are: 1. To compare the safety and tolerability of GM608 with placebo in a population of patients with early PD. 2. To field test the study procedures for feasibility and efficiency 3. To determine if there is any hint that injections of GM608 might slow the rate of clinical worsening of PD.
In this proposal the investigators have three Specific Aims using human patient populations as model systems; 1) identify a role for the Basal Ganglia (BG) in perceptual decision making; 2) determine whether the Basal Ganglia contribute to decision making under conditions of visual uncertainty; 3) determine whether the cerebellum plays a role in perceptual decision-making under conditions of visual uncertainty. The investigators designed experiments using healthy humans and humans with diseases known to affect the Basal Ganglia and the cerebellum, Parkinson's Disease, dystonia and non-dystonic cerebellar damage. With this approach the investigators will test the following hypotheses: 1) Patients with Parkinson's Disease and dystonia will have more difficulty than healthy controls making perceptual decisions when faced with sensory uncertainty; when sensory information is certain, patients will show improved decision-making but will still be impaired relative to healthy humans. Hypothesis 2: If ambiguous sensory information is aided by prior information, patients with Parkinson's Disease and dystonia will be unable to use the prior (bias/memory) information to inform their decisions. Hypothesis 3: Deep Brain Stimulation (DBS) of Basal Ganglia structures will improve the ability of patients to use prior information to inform their decisions when faced with sensory uncertainty. Hypothesis 4: Both cholinergic and dopaminergic medical therapies will improve the ability of patients to use prior information to inform their decisions. Hypothesis 5: Patients with non-dystonic cerebellar damage will be similar to healthy controls in performance of a perceptual decision making task in conditions of visual uncertainty. The overarching framework of this application is that the same mechanisms (D1 striatal synaptic plasticity) that operate in reward learning play a role in learning and using stimulus priors in a perceptual decision-making task when faced with uncertainty. Because Parkinson's Disease and dystonia share deficits in striatal circuitry, the patient deficits on this task will be similar. Because non-dystonic cerebellar patients do not have dysfunction of striatal circuits, they will show no deficits in the ability to use stimulus priors to guide choices in uncertain conditions. In the event these patients do show deficits, this is will provide evidence for an unexplored role for the cerebellum in perceptual decision-making.
The purpose of this study is to evaluate the safety and effectiveness of Boston Scientific's Vercise Deep Brain Stimulation (DBS) system in the treatment of patients with with advanced, levodopa-responsive bilateral Parkinson's disease (PD) which is not adequately controlled with medication.