View clinical trials related to Tauopathies.
Filter by:This is an open-label study to evaluate the performance of a novel tau imaging ligand in up to 36 subjects (12 AD, 3 FTD, 3 PSP, 3 CBS, 3 VCI and 12 HV). Subjects will be recruited from the patient population and healthy volunteers of Taiwan residents. This study protocol requires each subject to complete the following components: screening evaluation, brain MRI and 18F-PM-PBB3 PET imaging up to two sessions. The screening procedures will include neuropsychological assessments, vital signs, ECG, physical examinations and laboratory tests. In addition, 18F-AV-45 PET imaging result will be as a part of inclusion criteria to confirm presence of amyloid deposition in patients with clinically diagnosed probable AD or absence of amyloid deposition in FTD, VCI and HV subjects. Furthermore, 18F-AV-133 PET imaging data will also be as a part of inclusion criteria to confirm the diagnosis of PSP and CBS. All subjects will complete clinical assessments and clinical safety tests to ensure the subject is medically stable to complete the study protocol. The screening procedures will occur within 30 days prior to 18F-PMPBB3 PET imaging.
The goal of this study is to characterize tau kinetics and tau aggregation in the human CNS and to test the hypothesis that tau kinetics are altered (i.e. increased production, decreased clearance, and increased aggregation rate) in tauopathies.
This study seeks to evaluate the efficacy and safety of NA-83 in subjects with mild cognitive impairment due to Alzheimer's Disease
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.
The goal of this study is to identify the most reliable methods of analysis for tracking CBD, PSP, and o/vPSP over time. The results from this study may be used in the future to calculate statistical power for clinical drug trials. The study will also provide information about the relative value of novel imaging techniques for diagnosis, as well as the value of imaging techniques versus testing of blood, urine, and cerebrospinal fluid (CSF) 'biomarkers'.
This retrospective study is a more extensive, confirmatory analysis of the cognitive and functional outcomes initially seen in 2 groups of MCI/dementia patients in Springfield, MA and compares specialized dementia care and a comprehensive treatment approach versus usual care delivered in a non-specialist setting. The first group of patients (n= 328) was seen by a dementia specialist, who utilized a standardized assessment and treatment protocol (CNS). This included comprehensive identification and treatment of hypoxia, sleep-disorders, and other cognitively-impairing metabolic conditions as well as maximally- dosed FDA-approved medications for dementia, depression, and PBA. The second group of patients (n= 280) was seen by non-dementia specialists in the community and received usual care which did not include comprehensive assessment or treatment of underlying metabolic derangements or maximal utilization of currently available medications. This study, evaluating date from a larger cohort (n>800) of specialist-treated cognitively-impaired patients, will further examine the hypothesis that a comprehensive dementia treatment protocol yields cognitive stabilization and/or improvement using already available dementia drugs when compared with usual community care.
The study will investigate the ability of a new PET tracer, 18F-AV-1451, to detect depositions of a protein, called tau, in the brains of people with a mutation in the tau gene that causes deposition of the protein, and in people without the mutation. Up to three 18F-AV-1451 scans will be performed (one per year) on control subjects without MAPT mutations, presymptomatic mutation carriers, and symptomatic mutation carriers.
The overall goal of this imaging trial is to characterize [18F]MNI-815, a PET radioligand for imaging Tau.
This is a randomized, double-blind, placebo controlled, single ascending dose escalation, safety, tolerability, PK, PD and immunogenicity study of BMS-986168 administered by an intravenous infusion in healthy subjects.
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: 1. Patients with clinically definite PSP will present an increased uptake in basal ganglia, brainstem and cerebellum. 2. Patients with clinically defined MSA will not present specific uptake. 3. 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