View clinical trials related to Late Onset Alzheimer Disease.
Filter by:A phase 2, double-blind, randomized, placebo-controlled clinical trial to evaluate the safety and efficacy of Allopregnanolone as a regenerative therapeutic for Alzheimer's disease.
To afford urgent access to a potential-disease modifying treatment, Dr. Diana Kerwin, in partnership with CTD Holdings, the manufacturer of Trappsol (R) Cyclo(TM), will administer the product to a patient with Alzheimer's Disease who has no other disease-modifying treatment options.
Pharmacological treatment of AD is currently based on cholinesterase inhibitors (ChEI) and memantine, which have been shown to lead to modest, although effective, clinical benefits. Donepezil is a ChEI metabolized through the cytochrome P (CYP) 450, primarily by the 3A4 and 2D6 isoforms. The CYP2D6 gene presents polymorphisms that can alter its expression. The plasma therapeutic level ranges from 30 to 75 ng/mL, and 50% of acetylcholinesterase inhibition is achieved when the concentration reaches 15.6 ng/mL. An optimal plasma level is greater than 50 ng/mL. These polymorphisms may influence the individual's response to treatment with donepezil and the concentration of the drug in AD patients, without achieving the desired effect. However, most of the individuals are EM, i.e., the metabolism of the drug occurs according to the expected kinetics and is associated with the presence of one or two wild-type alleles. Objective: investigate the pattern of clinical response to donepezil in a group of patients with AD and AD with cerebrovascular disease (CVD) in relation to the plasmatic concentration of donepezil and polymorphisms of the CYP2D6 and apolipoprotein E (APOE) genes.
The overall goal of this project is to establish and validate biomarkers associated with the risk and progression of late onset Alzheimer's disease, mild cognitive impairment and cognitive decline. The investigators will use baseline and longitudinal measurements of plasma amyloid beta-40 and amyloid beta-42 to investigate the risk of developing mild cognitive impairment and late onset Alzheimer's disease, as well as the rates of cognitive decline and Alzheimer's disease progression. Participants will be selected on the basis of change in plasma amyloid beta levels over prior assessment intervals. The purpose of the study is to examine whether brain amyloid plaque load, which will be measured with positron emission tomography and x-ray computed tomography brain imaging using Florbetaben from Bayer, varies as a function of change in plasma levels of amyloid beta. The driving hypothesis of the study is that high plasma levels of amyloid beta are an antecedent indicator of increased risk of cognitive decline, mild cognitive impairment, and incident late onset Alzheimer's disease, and that declining plasma levels of amyloid beta are associated with the onset of cognitive decline. Further, high plasma levels of amyloid beta are related to increased levels of amyloid beta in the brain as measured by positron emission tomography positivity, and the specific pattern of positron emission tomography positivity and a decline in plasma amyloid beta over time are associated with the onset of cognitive decline associated with late onset Alzheimer's disease.
The purpose of the Alzheimer's Disease Genetics Study is to identify the genes that are responsible for causing Alzheimer's Disease (AD). One of the ways in which the risk factor genes for late onset AD can be investigated is by identifying and collecting genetic material from families with multiple members diagnosed with AD or dementia.