Active clinical trials for "Alzheimer Disease"

The study aims to investigate the effect of a long-term combined aerobic exercise and cognitive training program on cognitive function and blood exosomal synaptic protein levels in seniors at increased risk for Alzheimer's Disease.

This study focuses on the population of Alzheimer disease (AD). Based on Aβ(A)-Tau(T)-Vascular(V)-Neurodegeneration(N) (ATV(N))-AD evaluation system of NIA-AA Association, it can accurately diagnose and predict early AD. Positron emission tomography (PET) - magnetic resonance (MR) was used to perform Aβ、Tau molecular imaging, representing A and T in the system respectively; The quantitative detection of glucose metabolism in the brain by fluorodeoxyglucose PET (FDG-PET) can reflect the degree of neuronal damage (N); In addition, PET-MR can be used to synchronously evaluate the patients' vascular comorbidity (SVD load score) (V). Through the preliminary construction of this system, to clarify the central deposition pattern of Aβ、tau protein and the characteristics of FDG metabolism; To clarify the correlation between PET-MR imaging indexes and the progression of early cognitive impairment in AD, and to clarify the role of degeneration and vascular factors in the occurrence and development of AD; To provide a preliminary basis for the subsequent establishment of a molecular imaging model for the prognosis of early AD.

Modifying health behaviors like physical activity level, diet, stress, and mental activity level can lower risk for Alzheimer's disease, but many middle-aged and older adults find it difficult to sustain health behavior changes over the long term. This project will develop a new intervention that educates people about Alzheimer's disease risk factors and helps them understand how their personal health beliefs may prevent them from making long-lasting lifestyle changes. The goal is to help people sustain health behavior changes to prevent or delay the onset of Alzheimer's disease and related dementias.

Alzheimer Disease (AD) is a progressive brain disease generally known as senile dementia. Our proposed study will establish safety and pharmacokinetics of Meganatural-AZ GSPE in AD subjects. As secondary measures, we will also provide the essential human data to guide the design of future studies to test the efficacy of GSPE in mitigating cognitive deterioration in AD patients.

Compensatory aids (e.g., alarms, calendars) play an important supporting role when completing everyday tasks (e.g., appointments, medication management), and there is a growing body of scientific work suggesting that compensatory training improves daily functioning. However, traditional paper-based calendars and to-do-lists have limitations related to accumulation of information, difficulty retrieving information, and remembering to complete activities. Such limitations may be overcome using a digital format through organized digital files, search functions, and alarms. This pilot project proposes to train older adults at risk for cognitive decline to use the Digital Memory Notebook (DMN), a tablet-based application (app), to support everyday functioning. The primary goal is to obtain preliminary evidence that a 6-week, individual and group-based DMN training intervention results in demonstrable changes in target behaviors (e.g., goal-directed DMN use to support everyday activities) among older adults with mild cognitive impairment (MCI) and subjective cognitive complaints (SCC). Participants will complete a curriculum involving 2-hour weekly sessions for 6-weeks. Each week will cover a specific function of the DMN and will include standardized goal-setting and weekly homework targets. Following the 6-week intervention, participants will continue to use the DMN app for 4-weeks to evaluate stability. Participants will complete a questionnaire packet 1 week prior to the 6-week intervention, 1 week after the 6-week intervention, and 5 weeks following the 6-week intervention. MCI and SCC participants will complete separate 6-week individual or group interventions spaced two months apart at UCD.

This study aims to analyse, in vivo, the interplay between microglial activation and tau pathology in Alzheimer's disease (AD) using [18F]-DPA-714 and [18F]-Ro948 tracers by Position Emission Tomography (PET), and their consequences on synaptic density using [11C]-UCB-J, a recent PET radioligand. By coupling advanced neuroimaging techniques in AD patients, while comparing them to controls, we will be able to study, for the first time in humans, the interaction between neuroinflammation, tau pathology, synaptic density, and their impact on AD progression. Joint analyses of peripheral immune biomarkers, carried out as a secondary objective, will further aim at defining peripheral correlates of this interplay. Overall, we aim to refine AD subgroup classification in order to improve and to refine the design of new therapeutic trials.

Years before someone experiences the symptoms of Alzheimer's disease, a compound called amyloid beta (Aβ) builds up in the brain. Excess Aβ - directly or indirectly - causes many of the symptoms of Alzheimer's dementia. However, recent studies of the FDA-approved drugs lecanemab (Leqembi®) and aducanumab (Aduhelm®) indicate that removing Aβ from the brain doesn't stop Alzheimer's. Clearly, there are other problems that need to be fixed. The investigators are interested in the cause of Aβ buildup. Non-neuronal support cells, called glia, keep neurons healthy by regulating water and nutrient levels for the neurons. They also help clear Aβ away from neurons. Maybe Aβ builds up when glia are unhealthy. Glia are very hard to study in the brain. Luckily, the light-sensing part of the eye - the retina - is an extension of the brain. The investigators study glia in the retina to learn about glia in the brain. To study retinal glia, the investigators take pictures of the retina with optical coherence tomography (OCT). OCT is safe, painless, and is used in many eye clinics to look at the structure of the retina. When the investigators take OCT pictures under a bright light, and compare those to OCT pictures collected in darkness, it gives the investigators information about glial function. In a study published in 2020 ("Optical coherence tomography reveals light-dependent retinal responses in Alzheimer's disease") the investigators showed that this functional OCT measurement was different in people with Alzheimer's dementia, compared to age-matched healthy adults. The goal of this observational study is to compare people at a pre-dementia stage of Alzheimer's disease to people who do not have any signs at all of Alzheimer's disease. By "pre-dementia stage", the investigators mean people who are either cognitively normal, or have mild cognitive impairment, but have had a medical test that shows the chemical beginnings of Alzheimer's disease. Members of the comparison group will also be cognitively normal, or have mild cognitive impairment, but had a medical test that shows utterly no signs of Alzheimer's disease. The main question this study, is whether functional OCT can tell these two groups apart. If so, that would: Help build the case for glial health being important in the earliest stages of Alzheimer's, which in turn could lead to new treatment strategies, and Suggest that functional OCT might be used as an early (pre-dementia) screening test for Alzheimer's disease Participants will: undergo a brief eye exam (the investigators will not dilate pupils for this study) undergo a paper-and-pencil cognitive test (to help verify "normal" or "mild cognitive impairment" status) take brief one-page survey to collect demographic information (like age) permit limited access to pre-existing medical or research records (to verify the presence/absence of the chemical beginnings of Alzheimer's disease) take several OCT pictures of both eyes, in light and after 2 minutes of darkness (several rounds of images are taken) The expectation is that all study procedures will fit within 2 hours of one day.

The investigator has shown that improved cardiorespiratory fitness following an aerobic exercise program elicits cognitive benefit in elderly subjects and memory improvement in Alzheimer's disease (AD). The physiological mechanism may be related to exercise-mediated change in circulating factors that permeate the brain. The response to each individual bout of exercise (i.e. the acute exercise response) may differ between subjects and be key to driving brain benefit. In young populations, the acute response to exercise can last hours and affect brain glucose metabolism. However, the field knows little about this acute exercise response in AD. Most exercise intervention trials designed to prevent and slow AD, including our own (AG033673; AG034614; AG043962; AG049749; AG053952), assess biomarkers at two fasting time points: pre- and post-intervention. The acute exercise response in the brain and periphery likely varies between subjects and diagnoses and provide key information regarding mechanisms of benefit. Our primary goals are to characterize the acute exercise response to exercise in the brain (glucose metabolism) and periphery (biomarker response) in aging and AD. The investigator will identify relationships between exercise-related factors (i.e. heart rate, biomarkers) and change in brain metabolism and cognition. Understanding these mechanistic relationships will provide specific targets that can be used in future trials to develop individualized exercise prescriptions and maximize benefit. Accumulating evidence suggests that the exercise-related metabolite lactate is an understudied effector of brain health. Lactate is an essential fuel for neuronal function. It is supplied to neurons through glucose metabolism in nearby glia and from peripheral blood, since the brain is permeable to lactate. A drop in cerebral glucose metabolism is a marker of AD. Thus, supplying neurons directly with lactate for oxidation may supplement energy requirements in AD, as has been suggested with ketones. Importantly, circulating lactate levels rise during exercise. Repeated increases in systemic lactate (acute exercise response) may transiently spare glucose by providing an alternative fuel. With routine exercise, acute responses may elicit adaptations that facilitate the use of lactate beyond that which occurs during acute exercise and contribute to brain benefits observed during chronic exercise interventions. In younger populations, higher exercise intensity evokes a greater lactate response compared to lower intensities and elicits cognitive benefit. The investigator will achieve these goals through the following aim: Aim 1. Examine differences in lactate metabolism between diagnosis groups and the effect of lactate on cognitive performance. Increased blood lactate can reflect increased production or decreased uptake. This has never been compared in ND and AD. The investigator will use a "lactate clamp" procedure, where lactate is infused to concentrations that match those found during exercise, to characterize lactate turnover. The investigator will characterize cognitive performance following lactate infusion, independent of exercise factors. The investigators hypothesize that ND subjects (n=12) will use lactate more efficiently (greater uptake) than AD individuals (n=12). The investigator further hypothesize that cognitive performance will acutely improve after lactate infusion in ND and AD subjects. The overall goal is to characterize lactate metabolism, and its relationships with cognition. The KU ADC is a recognized leader in the study of exercise and metabolism in aged and AD populations, and puts the investigator in a strong position to successfully achieve these aims.

The study aims to investigate the effect of a long-term combined aerobic exercise and cognitive training program on cognitive function, daily function, psychosocial status, and neural plasticity in seniors with genetic susceptibility for Alzheimer's Disease.

The purpose of this research is to further investigate the potential of brain stiffness as a novel biomarker for Alzheimer's disease.