Active clinical trials for "Alzheimer Disease"

The purpose of this study is to evaluate the biodistribution, safety and tolerability of a single dose of [18F]GTP1 as a tau targeted radiopharmaceutical in healthy Japanese participants.

This project aims to examine the effect of a 5-month period supervised exercise intervention on brain, cognition, OMICs, Molecular Markers and functional status in older people at risk of mild cognitive impairment. Secondarily, the effect of this intervention on antioxidant capacity, lipid metabolism and glucose, physical health (functional capacity, blood pressure, body composition) and mental (quality of life and depression) will be studied, as well as other factors risk (genetic and biological) for the development of Alzheimer. A total of 100 people aged between 65 and 75 years old at risk of mild cognitive impairment will be randomly distributed in the supervised exercise intervention group (n = 50) and control group (n = 50). The design will include a 5-month intervention with measurements at pre and post intervention and a third measurement (retest) after 3 months of completion. The multicomponent supervised exercise program will include aerobic, strength, cognitive and coordinative-agility-balance works, and progression will be established in different load parameters (frequency, volume, intensity, density). Therefore, randomized controlled studies are needed to know the specific effect of dose-response considering the various dimensions in parallel such as neuroimaging, cognitive status and OMICS. This will allow us to understand from a comprehensive perspective the causes and mechanisms underlying the response. This project will significantly increase scientific knowledge about the role of exercise on brain as a therapeutic measure in people at risk of mild cognitive impairment from a multidimensional perspective. The project will have a significant impact at social and economic level by transferring the study findings to social and health setting by means of agents and networks provided for the project.

This randomized controlled trial is aimed at studying the effects of an eHealth intervention on improving metabolic control and other cardiovascular risk factors (obesity, lipidic profile and hypertension) as the approach to prevent or delay the process of cognitive impairment, and to reduce conversion rates to Alzheimer's disease (AD) in a sample of patients diagnosed of type 2 diabetes mellitus (T2D) and with mild cognitive impairment (MCI). For these purposes, the standard clinical treatment for this type of patients will be compared with two types of interventions (parallel groups): one aimed at promoting adherence to treatment through the use of a smart pillbox; and the other intervention will be based on the use of the smart pillbox plus and interactive digital platform allowing communication between patients and caregivers with healthcare professionals. Both interventions are targeted to improve adherence to treatment. The hypothesis is that the rate of conversion from MCI to AD will be higher in the control group than in the intervention groups (higher conversion rates are expected in control group, followed by the smart pillbox group, and lower conversion rates are expected in the group using the interactive digital platform and the smart pillbox).

This is an open-label study to evaluate the performance of a novel tau imaging ligand in up to 36 subjects (12 AD, 3 FTD, 3 PSP, 3 CBS, 3 VCI and 12 HV). Subjects will be recruited from the patient population and healthy volunteers of Taiwan residents. This study protocol requires each subject to complete the following components: screening evaluation, brain MRI and 18F-PM-PBB3 PET imaging up to two sessions. The screening procedures will include neuropsychological assessments, vital signs, ECG, physical examinations and laboratory tests. In addition, 18F-AV-45 PET imaging result will be as a part of inclusion criteria to confirm presence of amyloid deposition in patients with clinically diagnosed probable AD or absence of amyloid deposition in FTD, VCI and HV subjects. Furthermore, 18F-AV-133 PET imaging data will also be as a part of inclusion criteria to confirm the diagnosis of PSP and CBS. All subjects will complete clinical assessments and clinical safety tests to ensure the subject is medically stable to complete the study protocol. The screening procedures will occur within 30 days prior to 18F-PMPBB3 PET imaging.

The study aims to compare tau targeted radiotracers [18F]GTP1 and [18F]PI-2620 or [18F]MK-6240 in subjects with normal cognition or prodromal to moderate Alzheimer's disease (AD).

The study will be conducted by the Sponsor to evaluate the efficacy and safety of GV1001 (0.56 mg and 1.12 mg) administered subcutaneously as a treatment for moderate to severe Alzheimer's disease (AD). Studies using in vivo and in vitro AD models have shown that GV1001 inhibits neurotoxicity, apoptosis, and the production of reactive oxygen species induced by amyloid beta (Aβ) in neural stem cells by mimicking the extra-telomeric functions of human telomerase reverse transcriptase (hTERT). In nonclinical studies, using both mild (early stage) and severe (late stage) AD mouse models, GV1001 was shown to improve cognitive function and memory, as well as significantly reduce the amount of Aβ and tau proteins. The multifunctional effect of GV1001 makes it a promising therapeutic option for the treatment for AD. In a completed Phase 2 study conducted in Korea, GV1001 showed significant improvement in change from baseline of Severe Impairment Battery score at Week 24 and demonstrated a clinically acceptable safety profile in patients with moderate to severe AD.

This intervention is designed to promote enhanced use of compensation strategies including calendar and task list use, and organization systems, as well as increased engagement with brain health activities including physical exercise, cognitive activities, and stress reduction.

Two-year double-masked trial of over-the-counter dosage of naproxen sodium vs placebo in 200 cognitively normal participants with a parental or multiplex first-degree family history Alzheimer's disease (AD) dementia. Primary outcomes are decline in cognitive function and slope of change in a summary Alzheimer Progression Score derived from serial assessment of neuroimaging, biochemical, and sensori-neural biomarker indicators of pre-clinical disease -- all believed likely to reflect progress of preclinical AD in this high risk cohort. Approximately 2/3 of participants have volunteered also for serial lumbar punctures for analysis of cerebrospinal fluid. A two-year off-treatment delayed-washout phase is planned to examine sustained treatment effects and evidence of disease modification.

The 'Amyloid Cascade Hypothesis' posits that the accumulation of a peptide, amyloid beta (Aβ), in the brain is the initiating event in Alzheimer's disease (AD), however, the mechanisms involved are not well understood. Recent studies support the hypothesis that Aβ dynamics in the brain are influenced by the sleep-wake cycle, with increases in the production of soluble Aβ during wakefulness and decreases during non-rapid eye movement (NREM) sleep, and more specifically on NREM stage 3 (also called slow wave sleep [SWS]). These changes produce a consistent diurnal pattern in the cerebrospinal fluid (CSF) that has been documented in murine models and in humans. By better understanding this sleep-wake relationship the investigators hope to identify how sleep disorders accelerate the progression of AD in the elderly (which has been demonstrated by multiple epidemiological studies) and, in turn, identify novel therapeutic targets for AD prevention. The purpose of this study is to elucidate how soluble amyloid beta (Aβ) levels in the brain are influenced by the sleep-wake cycle in humans, and to test the directionality of this relationship through sleep disruption experiments. The investigators will test two models. The first model will test how, prior to amyloid deposition, brain soluble Aβ levels may be relatively increased in the elderly by two mechanisms: a) loss of total sleep time and SWS that occur with normal aging; and b) sleep disturbances such as Sleep Disordered Breathing (SDB) or insomnia that are common in late life (Aim 1). The second model will test how stage-specific sleep disruption may lead to increased CSF Aβ42 levels (Aim 2). A group of adults with diagnosed severe SDB and good continuous positive airway pressure (CPAP) compliance will be used to test this model sleep deprivation experiments using therapeutic CPAP vs. sham CPAP. This project will be the first to explore the protective effect of SWS on Aβ42 dynamics in a group of cognitively normal elderly subjects as well as the effect of acute sleep disruption by CPAP withdrawal on CSF Aβ42 levels in a well characterized clinical sample of severe obstructive SDB patients on treatment with CPAP. The results from this study will improve our understanding of the nature of the Aβ diurnal pattern and the brain consequences of full night sleep disruptions as well as sleep disruptions during specific stages of sleep.

This 2-part, open-label study was designed to investigate the safety, tolerability, and efficacy of [18F]MK-6240, a Positron Emission Tomography (PET) imaging agent, for the quantification of neurofibrillary tangle (NFT) deposition in the brain. Brain NFT deposition is a pathologic finding in Alzheimer's Disease (AD), with brain NFT density shown to correlate with the severity of cognitive impairment in AD. The objectives of the study include performing the following with respect to [18F]MK-6240 administered as a PET imaging agent: 1) assess safety and tolerability; 2) determine radiation safety profile; 3) determine optimal imaging protocol parameters for quantification of brain NFTs in AD; 4) compare tracer binding in brain PET scans from participants with AD, participants with amnestic mild cognitive impairment (MCI) and healthy elderly participants; and 5) evaluate intra-subject test-retest (T-RT) variability of tracer uptake in brain regions of interest.