View clinical trials related to Alzheimer Disease.
Filter by:Alzheimer's disease (AD) is associated with significant, progressive cognitive decline. Key defects in mitochondrial fuel metabolism insulin resistance, inflammation and decreased brain glucose uptake are linked to AD. This trial will investigate the effects of supplementing glycine and N-acetylcysteine vs. alanine as placebo on these defects in AD, and examine the effects on cognition.
This is a pilot RCT with equal arms: experimental arm and (wait list) control arm. All participants will be in the early stage of Alzheimer's disease and on stable medication. They will all continue with this medication for their 6 months participation. Experimental group will add weekly training on the experimental device, 5 days a week for 8 weeks. Training will involve therapeutic games aimed primarily at the memory cognitive domain. All participants will receive weekly calls from clinical coordinator and report on medication and overall health. Caregivers will also be enrolled so they support the trials.
The aim of this study is to create a repository of both cross-sectional and longitudinal data, including cognitive, linguistic, imaging and biofluid biological specimens, for neurodegenerative disease research and treatment.
The ketogenic diet (KD) is a metabolic shift, which stimulates the liver oxidation of fatty acids to produce ketone bodies. These ketone bodies represent an alternative fuel source for the brain. The benefits of KD in epilepsia have been demonstrated for decades. This diet may also provide benefits in Alzheimer's disease (AD) where neuronal glucose utilization declines from the early stage. Besides, the KD could decrease neuroinflammation, oxidative stress and enhance mitochondrial biogenesis. In murin models of AD, KD or Medium Chain Triglycerides consumption were associated with lower neuroinflammation but also with a diminution of neuropathologic features of AD (amyloid and tau lesions in the brain). Moreover, behavioural effets and improvements in memory and motor function have been highlighted. In humans, recent studies suggest cognitive benefits (memory, executive function) in AD, including in the Mild Cognitive Impairment (MCI) stage. The feasibility and the adherence to the diet proved to be correct, in small samples, in particular in MCI individuals over a short follow-up period (3 to 6 months). This study aims at examining the feasibility of a KD followed-up for one year in participants with early AD (N=70). Change in brain metabolism will be assessed using PET scan after 12 months, comparing KD with control diet. The effects on cognition, quality of life and daily living functioning will be analysed. The safety, nutritional changes and adhesion to the diet will be monitored throughout the study.
The incidence of AD dementia is increasing due to the aging population, putting a heavy burden on our society and economics. Exploring the mechanisms underlying SCD due to preclinical AD has scientific and clinical significance. However, it is challenging to construct and validate the preclinical diagnosis model of AD with fused multimodel information across culture/race. From the cooperation during the past five years, we have established cohorts by synchronized assessment, achieved consensus on SCD features extraction and made a breakthrough in the application of multiple parameter MRI with German collaborators. Therefore, in this project, SCD with and without amyloid pathology will be compared by clinical and cognitive data, genetics, blood and MRI biomarkers between the German and Chinese. Key features will be extracted and specific characteristics of SCD due to preclinical AD as well as risk factors for conversion between two countries will be clarified. Then the diagnosis model of preclinical AD in SCD will be established across culture/race based on radiogenomics, which will improve the current diagnostic system of AD. Through this project, the value of SCD in the etiologic, anatomical and quantitative diagnosis of preclinical AD will be identified to improve sensitivity and specificity of preclinical AD diagnosis in clinical practice.
High fat feeding (HFF) increases the risk of Alzheimer's disease (AD) but individuals who carry the AD risk gene E4 paradoxically improve after acute HFF. The investigators propose to further study this phenomenon with a clinical study to assess cerebral blood flow which can be measured by a technique called arterial spin labeling (ASL) on an MRI and is tightly related to brain metabolism.
The objective of the study is to determine the safety, feasibility, and efficacy of senolytics in older adults with amnestic mild cognitive impairment (MCI) or early-stage AD (Clinical Dementia Rating (CDR)=0.5 or 1) who are tau PET positive
The purpose of this study is to identify genetic factors that contribute to or cause dementia (loss of memory) and related disorders across all ages and ethnic groups. This includes a number of neurological diseases such as early and late-onset Alzheimer disease, mild cognitive impairment, and other dementias.
This study compares different music therapy (MT) experiences and their impact on memory and language in patients with Alzheimer's disease and Mild Cognitive Impairment. The 12-month study will assess the role of common experiences involving familiar music and other pleasant events (blinded control) to benefit cognition and measure the quality of life for people with Alzheimer's disease and Mild Cognitive Impairment. Following screening, all participants will meet with a licensed music therapist at the first study visit. Thereafter, each group will have an individualized schedule of follow-up telephone calls and visits. Screening for the study and participation in the study intervention can be completed in-person or from your home, if you do not live in the area.
Alzheimer's disease (AD) is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and, eventually, the ability to function independently. Despite the significant effort to understand the basic biology of the disease and pharmaceutical advances to develop drugs, there is no effective therapy available to treat AD or slow the disease progression. β-amyloid accumulation outside brain cells and abnormal accumulations of tau protein inside neurons are taught to be two main changes in the brain that lead to AD. Progressive accumulation of β-amyloid interferes with the neuron-to-neuron communication at synapses, contributing to neural cell death. Also, tau tangles block the transport of nutrients and other essential molecules into the neurons. Many molecules have been shown to inhibit amyloid aggregation. The anti-amyloidogenic activity of trehalose was confirmed in both in vitro and in vivo studies and its inhibitory effects on β-amyloid formation in AD have also been demonstrated. Trehalose is a non-toxic disaccharide and no dose-dependent adverse effects were seen in any of the safety studies. It can act as a chemical chaperone and stabilizes the natively folded structure of protein and also trehalose has been identified as an autophagy inducer and promotes the clearance of aggregated proteins. Therefore, trehalose could be a valuable candidate for the treatment and prevention of amyloid-related disease. Based on the proposed hypothesis, this study aim to investigate the potential efficacy of trehalose administration in patients with AD.