View clinical trials related to Huntington Disease.
Filter by:This study is to compare the pharmacokinetics of Dimebon in subjects with severe renal impairment to subjects with normal renal function after oral administration of a single oral 20-mg dose of Dimebon. This study is also to assess the safety and tolerability of a single oral 20-mg dose of Dimebon in subjects with severe renal impairment and subjects with normal renal function.
This drug-drug interaction study is being conducted to evaluate the potential effect of Dimebon on the pharmacokinetics on dextromethorphan, a probe substrate of the cytochrome P450 2D6 (CYP2D6) enzyme, after multiple dose administration to healthy adult subjects.
The purpose of this study is to determine if ACR16 is effective and safe in the symptomatic treatment of Huntington's Disease.
The pace of basic science research defining the mechanisms of selective neuronal degeneration in Huntington disease (HD) has far exceeded the pace of translation of this information into clinically effective treatments for the disease. One reason for this bottleneck between bench and bedside is the paucity of available surrogate markers for HD. Identification of surrogate markers is critical for the design of future clinical trials. Such markers could provide a reliable signal of early brain dysfunction in HD and could be used as a biomarker in trials of agents that could prevent onset or delay progression of disease. Frontal-subcortical networks are known to be affected in HD and contribute to the cognitive dysfunction characteristic of the disease. Quantitative EEG (QEEG) can be used to assess the integrity of this circuitry; characteristic QEEG abnormalities long have been known to be present in the early stages of the illness (Bylsma et al., 1994). More recent research has suggested that a comprehensive topographic approach to QEEG analysis may reveal additional changes in brain activity (Bellotti et al., 2004) that may be indicative of subclinical disease (de Tommaso et al., 2003). This proposal aims to determine whether quantitative EEG techniques can be used to identify HD-specific abnormalities and thus serve as surrogate markers of disease. The goals of this pilot project are three-fold. First, we will determine if there are QEEG differences between normal control subjects and those with mild or moderate HD. Second, we will examine associations between severity of HD and the QEEG differences detected and determine if these QEEG differences are present when comparing the least affected HD subjects and normal controls. Third, we will examine associations between QEEG variables of interest and other clinical variables, including age of onset of symptoms, number of CAG repeats, severity of motor and behavioral symptoms as measured by the Unified Huntington Disease Rating Scale (UHDRS) subscores, and severity of cognitive impairment as measured by the cognitive subscore of the UHDRS and Mini-Mental State Examination (MMSE).
The purpose of this study is to determine if ACR16 is effective and safe in the symptomatic treatment of Huntington's disease.
The study is designed to collect data regarding the clinical course and outcome of patients suffering from memory disorders. Visits are charged to the individual's insurance inclusive of Medicare. Patients benefit from expert evaluation and treatment recommendations. Participants may be eligible for participation in experimental treatments in the future.
To determine if memantine in doses of 10 mg BID affects memory, cognition, and behavior in patients with Huntington's disease (HD).
Huntington's disease (HD) is autosomal dominant neurodegenerative disease, starting in average (with high variability) in the fourth decade. The disease progression is classically characterized by a cognitive deterioration (cortical-frontal dementia), motor disorders (associating chorea, dystonia and bradykinesia), psychiatric disturbances (combining depression and irritability) and metabolic disorder (cachexia). The disease is fatal within 15 to 20 years in most patients. HD has no cure. Neuroleptics are the main drug used and the only to demonstrate its efficacy on chorea in clinical trials. But neuroleptics have also beneficial and adverse effects on other disease characteristics (motor, psychiatric, cognitive or metabolic). Their profile between beneficial and adverse effects could be different according the neuroleptics and their classification. The aim of this study is to compare beneficial and adverse effects of 3 different neuroleptics in HD.
PRECREST is a two phase protocol for Huntington's disease in which 60 premanifest and at-risk subjects will first be randomized into a double blind placebo controlled dose titration study bringing them to 30 grams daily or their highest tolerated dose. This phase will establish the highest tolerable doses in premanifest HD and permit the detection of toxicity and intolerability with attribution to active compound versus placebo, and enable a dose response assessment of biomarkers. In the second phase, all subjects will enter a year long open-label treatment on 30 grams daily (or their highest dose) of creatine to assess long term exposure to high dose creatine and its long term impact on various biomarkers.
This exploratory study will examine ways in which individuals approach a positive genetic test for Huntington Disease (HD). HD is a neurodegenerative disorder that causes emotional, cognitive, and movement problems, and currently there is no way to prevent, stop or reverse the progression of the disease. It is passed down through a mutation in a normal gene, and each child of an HD parent has a 50-50 chance of inheriting the HD gene. The study is designed to explore how individuals adjust to their new genetic status and evaluate any perceived mental or emotional barriers to that adjustment. Currently, little is known about how individuals come to terms with a positive genetic test result for a condition that has no known cure or effective treatment. The results of this study may give health care providers and counselors more information about how to help patients who are at risk for developing HD make sense of their new genetic status. Candidates will be prescreened and referred to the study by clinics that specialize in genetic testing and counseling. Candidates must be 18 years old or older and must have received a positive genetic test result for HD at least one month prior to the study. They must also perceive themselves to be asymptomatic-that is, without existing HD symptoms. During the study, participants will be interviewed and asked a series of questions about their decision to pursue testing, their life since the testing, and the things that they have found helpful or unhelpful since receiving the test results. The interviews will be recorded and will last approximately 60 minutes. Participants also will receive a follow-up phone call within two to three days to ensure their general psychological well-being after the interview.