View clinical trials related to Alzheimer's Disease.
Filter by:Alzheimer's disease (AD) is a major public health problem due to its socio-economic weight. An early diagnosis of AD is urgently needed as it would constitute a determinant breakthrough from a social, financial and research standpoints. Therefore, the investigators need predictive markers of AD, and neuroimaging is a particularly promising tool, especially when using complementary neuroimaging techniques and a longitudinal design, allowing to assess the relationships between the different biomarkers of the disease, their dynamic and their chronology.
Alzheimer's disease (AD) has a prolonged prodromal phase before the stage of dementia. Subtle executive cognitive function deficits can be detected at this early pre-dementia phase, more than 10 years before dementia. Among them, the digit symbol substitution task (DSST) has been shown to be altered very early, up to 13 years before dementia. This test, as many others executive function tests, requires a fine control of visuomotor coordination. Like executive functions, eye movements, particularly voluntary-guided saccades, are under the control of the frontal lobe and fronto-parietal networks. Previous studies have shown a deterioration of voluntary saccades in AD using various paradigms. There are no data in prodromal AD, although the pathological process of the disease affects very early brain structures implicated in saccades execution (eg. caudate nucleus and pre-cuneus).
Filgrastim (G-CSF) is widely used for treatment of patients who have a deficiency of white blood cells. It is also routinely used to stimulate and mobilize stem/progenitor cells for bone marrow transplantation. In studies of thousands of healthy donor subjects treated with G-CSF, the side-effects profile has been reported to be mild and reversible. Currently, G-CSF is under investigation in clinical trials in Germany and the US that aim to enhance recovery from strokes and heart attacks. In animal studies, G-CSF has been observed to improve cognitive performance and to markedly reduce amyloid deposition in hippocampus and entorhinal cortex in a mouse model of Alzheimer's Disease (AD). Since this drug is being used safely in many people throughout the world, the investigators hypothesize that it will also be safe to give to patients with Alzheimer's disease and that it may improve some aspects of memory and thinking. The present pilot study has two goals or objectives: 1) to investigate the effects of a five day schedule of Filgrastim administration on cognitive function and 2) to assess its tolerability and safety in a small group (12 patients) with mild to moderate stage AD. Patients who are eligible for the study will be randomly assigned to one of two groups (n=6 per group). One group will receive a five-day course of Filgrastim injections and the other group of subjects will receive vehicle injections (solution without drug). At the end of the first phase of the study (week 8), the groups will cross over to receive either vehicle or Filgrastim as appropriate. In this way all subjects will have received the active medication by the end of the study. After the study is finished the investigators should know whether or not Filgrastim improves some aspects of thinking and memory. And the investigators should know whether or not it is safe to give this medication to patients with Alzheimer's disease. To ensure that the drug is safe, a Safety Monitoring Committee will oversee the entire study. They will review all laboratory data, including complete blood counts, serum chemistry, EKGs and adverse events.
To evaluate the tolerability, safety and efficacy of 3-step titration versus 1-step titration of Rivastigmine patch in the Japanese population.
This study will test the use of venlafaxine to treat the depression in Alzheimer's Disease. Venlafaxine works by increasing natural substances in the brain (serotonin and norepinephrine) that help maintain mental balance. Alzheimer's disease (AD) is the commonest neurodegenerative disease of aging and the cause of major financial and emotional burden to patients, families and caregivers, and society. Depression is a very common symptom of AD, affecting as many as 50% of patients over their illness. Depression in AD (Alzheimer's disease) contributes greatly to patient disability and caregiver distress. Neither psychosocial interventions nor psychotropic medications have proven effective to date for the treatment of depression in AD.Venlafaxine is approved by the U.S. Food and Drug Administration (FDA) for the treatment of major depression but it is not known whether or not it can help depression in Alzheimer's Disease.
Biomarkers of Alzheimer's disease (AD) occupy an essential place in recently formulated diagnostic criteria for AD where their role is to identify the pathophysiological processes underlying cognitive impairment or to predict time to dementia. Three of these biomarkers are brain imaging tests (amyloid PET, fludeoxyglucose (FDG) PET, and structural MRI). In order to effectively use AD biomarkers for diagnostic and prognostic purposes, continuous values much be divided into normal and abnormal ranges. This requires that a cut point(s) be established in the continuous distribution of values for each biomarker. The investigators objective in this proposal is to obtain imaging biomarker data in a group of individuals who are appropriate for establishing normative values for AD biomarkers. The investigators believe the most valid approach to establishing biomarker cut points is to base them on the upper bound of the range observed in young to early-middle-age subjects in whom the presence of occult AD pathology is extremely unlikely. Based on a large volume of community-based autopsy data, that upper age limit would be about 50 years old. The lower age bound for a group of subjects used to establish normative AD biomarker values would have to be based on considerations of brain maturation, which may continue into the middle- to late-20s. Thus, taking the above into consideration, the ideal age range for establishing normative AD imaging biomarker data (amyloid PET, FDG PET, and structural MRI) may be ages 30-49 years old.
The intent of this research protocol is to test the equivalency of two amyloid imaging drugs (C11 Pittsburgh Compound B and F18 Flutemetamol). The investigators hypothesize that there will be no significant difference in the distribution of the agents to areas of amyloid deposition in the brain or to other normal brain structures. Recent data have shown similarity in the distribution of the drugs in subjects with AD or mild cognitive impairment (MCI). No comparison data of the two PET drugs in normal subjects has been published. It is important to understand differences in the images and biodistribution from the two drugs in normal subjects as nonspecific accumulation of the drugs in brain structures such as white matter appear to differ slightly and could affect image performance. The current clinical functional imaging standard for patients with indeterminate cognitive impairment is FDG PET. To allow a comparison of the PET amyloid imaging compounds with FDG PET, FDG PET scans will also be important to acquire in the subjects for comparison.
The purpose of the study is to evaluate the safety and tolerability of ascending oral doses of CHF 5074 after prolonged administration to patients with mild cognitive impairment.
Subjects will be adults aged 50 to 85 years who have subjective memory complaints and mild cognitive impairment or mild dementia due to Alzheimer's disease (AD). Subjects taking thyroxine or thyroid supplements and subjects receiving an acetylcholinesterase inhibitor (AChEI) and/or memantine for AD must be on a stable dose for at least 12 weeks prior to Screening and remain on their stable dose throughout the trial. Subjects will receive placebo or a single oral dose of E2609. Safety assessments will be conducted. Additionally, the pharmacokinetics of E2609 and drug effects will be evaluated using cerebrospinal fluid biomarkers and cognitive and psychological measures.
NMDA activation plays an important role in learning and memory. NMDA receptors were found to decrease in the frontal lobe and hippocampus of Alzheimer's disease and mild cognitive function impairment. This study is a randomized, double-blind, placebo-controlled drug trial. All patients will be allocated randomly to 2 groups: (1) NMDA enhancer: DAOI-B group (starting dose: 250-500 mg/d); (2) placebo group. The study period is 24 weeks. The investigators hypothesize that DAOI-B may yield better efficacy than placebo for cognitive function in patients with mild cognitive impairment or mild Alzheimer's disease.