Active clinical trials for "Parkinsonian Disorders"

The aims of this study are: 18F-THK5351 PET(Positron Emission Tomography) can defect the tau burden in PSP(Progressive Supranuclear Palsy) and CBS (Corticobasal syndrome)correlating with the known NFT(neurofibrillary tangles) topology of those diseases, 18F-THK5351 PET will differentiate subjects with suspected tauopathy due to PSP and CBS from subjects with suspected synucleinopathy due to idiopathic PD(Parkinson's disease). The distribution of PHF(paired helical filament) tau burden will correlate with specific motor and cognitive features of PSP and CBS; and regional PHF tau burden will be associated with cortical thinning. Together, these efforts will establish the potential for developing 18F-THK5351 PET imaging as a biomarker and diagnostic tool for the parkinsonian tauopathies.

This study involves study participants who have been clinically diagnosed with parkinsonian syndrome or who are at-risk for parkinsonian syndrome, have a family history of parkinsonian syndrome or exposure to environmental toxins potentially associated with parkinsonian syndrome. Participants will have brain imaging to assess dopamine transporter density. The imaging data coupled with family history and environmental exposure data may provide important information about potential risk factors for parkinsonian syndrome.

This study assesses dopamine transporter density using single photon emission computed tomography (SPECT) brain imaging with an investigational radiopharmaceutical, [123I]ß-CIT, in research participants with Parkinson's disease.

Based on previous promising results, the next step for the validation of a multimodal MRI method in diagnosis and follow up of patients reached by parkinsonian syndromes is (i) to test whether the multimodal neuroimaging is able to discriminate at the individual level, patients with multiple system atrophy parkinsonism (MSA) and patients with idiopathic Parkinson's disease (PD) (ii) to determine whether the method is sensitive to measure changes over time for the two diseases, according to imaging, neuropsychological and other clinical data. Patients will be compared with healthy controls.

This study evaluates the effect of the need to void on parkinsonian gait

The PET tracer [F18]-FDDNP has a specific affinity for lesions containing tau protein. The study consists of two phases: In the first (cross-sectional) phase it will be assessed the uptake of [18F]-FDDNP in 10 cases with progressive supranuclear palsy (PSP, a tauopathy) en 10 with multi-system atrophy (MSA, a non-tauopathy), along with 20 individuals with Unclassifiable Parkinsonism, as previously defined in a European cohort study. In the second (longitudinal) phase it will be prospectively followed the 20 unclassifiable patients (at 6, 12 and 18 months) by means of validated scales and accepted diagnostic criteria in order to try to correlate their eventual clinical diagnosis with baseline PET findings. On this basis, we endeavour to estimate the ability of this technique to detect in vivo underlying tau pathology in subjects initially unclassifiable on clinical grounds. We hypothesized that: Patients with clinically definite PSP will present an increased uptake in basal ganglia, brainstem and cerebellum. Patients with clinically defined MSA will not present specific uptake. Part of unclassifiable patients with parkinsonism will present a pattern of uptake similar to patients with clinically defined PSP and this part along the clinical follow-up will be meet clinical criteria for diagnose of PSP

Parkinson's disease (PD) is a progressive neurological disorder that is increasingly common with age, with the incidence rising from approximately 4 people per 10,000 in their forties to 2 in 100 over the age of eighty. Our understanding of the causes of PD has rapidly developed in the past two decades, but this has not yet translated into any clinically established neuroprotective treatment that slows disease progression. There is a growing consensus that the failure of previous efforts is mainly due to the causative diversity of PD i.e. that PD may have many different causes. For example, it is known that variants in mitochondrial (cellular power house) genes can cause specific forms of PD and this may be relevant to other forms of PD. The aim of this study is to attempt to group PD patients based on markers of biochemical dysfunction (e.g. into groups of patients that do and those who do not have evidence of mitochondrial dysfunction) to aid in the development of new candidate neuro-protective compounds. The investigators hope by grouping people with Parkinson's into those with and without impaired mitochondrial function the investigators will be better able to develop more targeted treatments aimed at protecting further loss of brain cells that occurs in Parkinson's disease. To achieve this the investigators will study people, in two study sites in London, with both genetic forms of PD and those with idiopathic PD (i.e. those where there is not a known genetic variant causing PD), as well as a healthy control group. All groups will undergo standardised clinical assessment to collect information on several aspects of their condition (e.g. disease severity, memory problems and sleep problems). Participants will be asked to provide blood, urine and optionally cerebrospinal fluid & skin samples from which various biochemical assays and genetic analysis will be performed in attempt to group participants based on the results of these tests. The study is funded for 3 years with participants being asked to attend for up to 3 study visits each over this time period.

The spinocerebellar ataxias (SCAs) are a genetically heterogeneous group of dominantly inherited progressive ataxia disorders. More than 30 different gene loci have been identified so far. The most common SCAs, which together account for more than half of all affected families, are SCA1, SCA2, SCA3, and SCA6. Each of these disorders is caused by a translated CAG repeat expansion mutation. SCA1, SCA2, and SCA3 usually have an onset between 30 and 40, and SCA6 usually begins at the age of 50 to 60. In addition to progressive ataxia, SCA1, SCA2, and SCA3 frequently present with additional non-ataxic symptoms, including parkinsonism. Carbidopa/levodopa was found to have a good therapeutic effect on parkinsonism. The SCA6 used to be considered a pure cerebellar disorder. However, a recent large study on natural history of SCAs found that patients with SCA6 often had nonataxia symptoms, an observation that challenges the view that SCA6 is a purely cerebellar disorder. Parkinsonism in SCA6 was rarely reported, except in a case serial, or a small size study in Korean patients. Dopamine transporter (DAT) is a very reliable dopaminergic neuronal marker. Reduction in DAT density detected by I123 SPECT DaTscanTM in the dopaminergic neuron terminal striatum was reported in one small size study consisting of eight SCA6 patients in Korea. There was also a PET study using different radioligand for DAT in a small group of SCA6 patients in Germany, which found sub-clinical change in DAT density in some patients with SCA6. There has been no study so far in the US on parkinsonism and other non-ataxia spectrum and striatal dopaminergic damage in SCA6, probably because non-ataxia feature of SCA6 hasn't received much attention, and also because DaTscanTM hasn't been clinically available in US until recently. The only two published studies on SCA6 and DAT were from Korea and Germany, which were of small subject size. There has been no treatment available for SCA6 so far. Our hypothesis is that parkinsonism and other non-ataxia spectrum and striatal dopaminergic neurodegeneration are part of the SCA6 disease spectrum.

The aim of this study is to determine whether a significant reduction in the total level of alpha-synuclein and significant increase in the oligomeric form of alpha-synuclein and therefore the ratio oligomeric:total alpha-synuclein occurs in patients with Parkinson disease compared to patients with drug-induced parkinsonian syndrome.

This will be two separate but identical studies: ALSE-A-02a, ALSE-A02b. Each study is designed to evaluate the diagnostic accuracy and safety of a single dose of 123I-ALTROPANE® in subjects with upper extremity tremor for less than three years. Currently, no radiopharmaceutical diagnostic imaging agent has been approved by the FDA in the U.S. for use in diagnosing Parkinson disease and related Parkinsonian syndromes. The diagnosis of Parkinsonian syndromes in the U.S. is based on clinical criteria only. The goal is to demonstrate that 123I-ALTROPANE® paired with SPECT imaging permits a more accurate early diagnosis of Parkinson disease than a clinical diagnosis by a general neurologist.