View clinical trials related to Alzheimer Disease.
Filter by:The purpose of this study is to examine the safety, tolerability, pharmacokinetics, pharmacodynamics, and immunogenicity of a single dose of PF-04360365 in Japanese subjects with mild to moderate Alzheimer's Disease.
Alzheimer's disease (AD) is a fatal degenerative disease of the brain for which there is no cure. AD causes brain cells to die. AD is thought to be caused by an excess of beta-amyloid (β-amyloid), a sticky protein in the brain that forms amyloid plaques. At autopsy, AD patients are required to have these amyloid plaques in the brain in order to have a definitive diagnosis of AD. Inhibiting the enzyme gamma-secretase (γ-secretase) lowers the production of β-amyloid. Semagacestat (LY450139) is a functional γ-secretase inhibitor and was shown to lower β-amyloid in blood and spinal fluid in humans tested thus far and in blood, spinal fluid, and brain in animals tested thus far. This study used several different tests to measure the effect of semagacestat on both β-amyloid and amyloid plaques for some participants. The build-up of amyloid plaques was measured by a brain scan that takes a picture of amyloid plaques in the brain. Other tests measured the overall function of the brain and brain size in some participants. In this trial, participants who initially received placebo (inactive sugar pill) were, at a certain point in the study, switched over to active drug, semagacestat. In other words, all participants could eventually receive active drug. Participation could last approximately 2 years. Participants taking approved AD medications were permitted to participate in this study and continue taking these medications during the study. All participants who completed this study had the option to continue receiving semagacestat by participating in an open-label study. Preliminary results from this study (H6L-MC-LFAN [LFAN]) and another similar study (H6L-MC-LFBC [LFBC; NCT00762411]) showed semagacestat did not slow disease progression and was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living. Study drug was stopped in all studies. Studies LFAN, LFBC, and open-label H6L-MC-LFBF (LFBF; NCT01035138) were amended to continue collecting safety data, including cognitive scores, for at least 7 months. The Clinical Trial Registry (CTR) will reflect results of analyses from the original LFAN protocol in addition to those from the amended LFAN protocol.
The purpose of this study is to collect data on the effects of behavioral interventions for memory and communication deficits in persons taking cholinesterase inhibitors compared with the effects of cholinesterase inhibitors alone. Initial testing will include a written case history, tests of communication skills, and interviews with the participants, family, and staff caregivers to help select potential goals for treatment. Participants will be randomly selected to participate in Group A (control) or Group B (intervention). Group A will use a Caregiver Checklist for eight weeks to identify any increase or decrease in the occurrence of the identified communication deficits. Group B will have 16 treatment sessions by a Speech Language Pathologist during the eight-week period. A post test will be administered to all participants.
We expect the results of this pilot study to justify a larger study that follows people to determine if certain tests of memory and attention, performed while sleepiness is induced by a single dose of lorazepam (a widely used anti-anxiety medication) could predict an individual's risk of developing AD. We plan to compare cognitively normal people who possess a common gene that increases risk for AD— the apolipoprotein E (APOE) e4 allele—to individuals without this gene. We hypothesize that a single 2 mg dose of lorazepam will cause more cognitive impairment in carriers of the APOE e4 allele than in noncarriers, and that the carriers will recover more slowly from these impairments than noncarriers.
This study will evaluate a handheld event-related potential (ERP) testing device from Neuronetrix, Inc. as a method to collect ERP data in an outpatient setting. An ERP system records electrical signals at the scalp that are produced by the brain when performing cognitive tasks. By doing this study, we hope to evaluate various performance parameters of the COGNISION(TM) system.
To determine which parts of the brain are involved in insulin-related memory improvement in early Alzheimer's disease and cognitively normal older adults.
The purpose of this study is to determine whether nicotinamide, or vitamin B3, is safe and effective in the treatment of Alzheimer's disease.
This is a multicenter, double-blind, placebo controlled, randomized, outpatient, multiple dose study in male and female patients ages 50 to less than 89 years with mild to moderate AD. Approximately 200 study sites in the US and Canada will be involved. Patients will be randomized to receive either bapineuzumab or placebo. Each patient's participation will last approximately 1.5 years. Bapineuzumab is a humanized monoclonal antibody, which binds to and clears beta amyloid peptide, and is designed to provide antibodies to beta amyloid directly to the patient.
This is a multicenter, double-blind, placebo controlled, randomized, outpatient multiple dose study in male and female patients ages 50 to less than 89 years with mild to moderate AD. Approximately 230 study sites in the US and Canada and up to 35 sites outside of North America will be involved. Patients will be randomized to receive either bapineuzumab or placebo. Each patient's participation will last approximately 1.5 years. Bapineuzumab is a humanized monoclonal antibody, which binds to and clears beta amyloid peptide, and is designed to provide antibodies to beta amyloid directly to the patient.
This is a study to determine the effectiveness and safety of donepezil hydrochloride (E2020) used to treat residents of assisted living facilities diagnosed with mild, moderate, or severe stage Alzheimer's disease.