Active clinical trials for "Alzheimer Disease"

The purpose of this project is to investigate the role of both neural inflammation and pre-existing neurodegenerative pathology in the risk and pathogenesis of post-operative cognitive dysfunction (POCD). To achieve this goal, the investigators will combine blood and cerebrospinal fluid (CSF) sampling, standardized cognitive tests, and dynamic neurophysiological markers of cortical network dysfunction in the form of event-related potentials (ERPs), to assess the link between neurodegeneration and neuroinflammation in the pathogenesis of POCD.

The researchers plain to build a large-scale, longitudinal, prospective cohort characterized by TCM dampness syndrome. With the biobank of this cohort the investigators want to find the causality between TCM dampness syndrome and clinical chronic diseases and a new way to treat clinical disease.

In this study, a total of 60 AD patients with Aβ deposition will beenrolled.Qualified subjects will complete PET imaging scan of Tau imaging agent inXuanwuHospital, and each subject will receive three of the following five imaging agents: PI-2620, APN1607, AV1451, RO948 or GTP1.The imaging time interval between the two tracers should be at least 4 days but less than 4 weeks. All PET scans of each subject were completed within 3 months.To compare the different Tau tracers' binding ability (SUVR or Tau distribution change) of the same subject in AD population. Obtain the safety data of each tracer after injection.

The Longitudinal Early-onset Alzheimer's Disease Study (LEADS) is a non-randomized, natural history, non-treatment study designed to look at disease progression in individuals with early onset cognitive impairment. Clinical, cognitive, imaging, biomarker, and genetic characteristics will be assessed across three cohorts: (1) early onset Alzheimer's Disease (EOAD) participants, (2) early onset non-Alzheimer's Disease (EOnonAD) participants, and (3) cognitively normal (CN) control participants.

The main objectives for this study are: To investigate novel, non-invasive ocular measurements including optical coherence tomography and eye tracking in a cross-sectional study of participants with various neurodegenerative dementias against standard cognitive assessments and brain imaging measures; and To assess the potential utility of ocular assessments for early detection in the pre-dementia, i.e. the so-called Mild Cognitive Impairment (MCI) stage, across the common neurodegenerative dementia syndromes and, Vascular Cognitive Impairment (VCI) due to small vessel disease (SVD). To determine the prevalence and relevance of amyloid uptake on PET scanning across the dementias most commonly associated with amyloidosis. Specifically we aim to examine correlations with amyloid uptake status in patients symptomatic from the most common proteinopathies (ie amyloid, tau, synuclein) combined in varying degrees with the most common vasculopathies (ie small vessel disease) using multimodal structural and functional imaging, cognitive behavioral, and gait and balance measures, taking into account genetic risk markers (particularly apolipoprotein E genotypes) and fluid biomarkers ( eg cytokines, oxidative stress, lipidomics).

Alzheimer´s disease (AD) in one of the most important causes of dementia and poses a considerable challenge in health care. Today, criteria for the diagnosis and the follow up of patients with AD mainly rely either on subjective tests or invasive methods. This limits the general applicability of the latter test for population screening and underlines the need for the identification of easily accessible tools for the identification of high-risk subjects. Because of its unique optical properties, the eye offers the possibility of the non-invasive assessment of both structural and functional alterations in neuronal tissue. As the neuro-retina is part of the brain, it does not come as a surprise that neuro-degenerative changes in the brain are accompanied by structural and possibly also functional changes in the neuro-retina and the ocular vasculature. The current study seeks to test the hypothesis that beside the known anatomical changes, also functional changes can be detected in the retina of patients with AD. For this purpose, flicker light induced hyperemia will be measured in the retina as a functional test to assess the coupling between neural activity and blood flow. Further, structural parameters such as retinal nerve fiber layer thickness and function parameters such as ocular blood flow and retinal oxygenation will be assessed and compared to age and sex matched controls.

A prospective and retrospective cohort study of about five years will be performed on blood and cerebrospinal fluid samples taken for diagnostic reasons from recruited patients within the Neuromed Neurology Unit. Subjects with other chronic neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD), and healthy subjects subjected to blood sampling and / or lumbar puncture for clinical reasons will be recruited As control groups.

Efforts to find treatments for AD have yielded only modest benefits, likely because longstanding AD pathological processes induce irreversible neurological compromise. These processes begin years before the onset of clinical symptoms. This possibility has been incorporated into a model describing stages of AD development, articulated by the NIA/Alzheimer's Association preclinical workgroup of which the Co-Director of the Kulynych Alzheimer's Research Center, Dr. Suzanne Craft, was a member. According to this model, the best hope for countermanding the effects of AD lies in intervening at the earliest possible point in the pathological cascade. There are several important ongoing efforts in adults with preclinical AD that directly target amyloid aggregation. Although this strategy addresses an important aspect of the AD pathological cascade, we believe that addressing metabolic dysfunction affecting glucose and insulin regulation offers a complementary approach, in that it may reduce amyloid burden and toxicity, while also directly enhancing synaptic health, brain metabolism, tau regulation and neurovascular function. The purpose of the ADCC is to identify and characterize early risk factors that predict cognitive decline and dementia in asymptomatic adults and adults with early signs of cognitive impairment. The data obtained from this study, collected at enrollment and follow-up will allow us to examine disease trajectory in individuals with and without prediabetes and other measures of glucoregulatory dysfunction in this process. The enrollees, who will be well-characterized with regard to cognitive and metabolic status through ADCC assessments, will provide an important resource for other local (institution) and national investigations. Data collected from participants enrolled in the ADCC will be stored indefinitely for future investigations.

Age-related sleep changes and common sleep disorders like obstructive sleep apnea (OSA) may increase amyloid burden and represent risk factors for cognitive decline in the elderly. We will directly interrogate the brain using a 2-night nocturnal polysomnography (NPSG) and amyloid deposition using C-PiB PET/MR both at baseline and at the 24-month follow-up. This study has the potential to identify the mechanisms by which age-related sleep changes contribute to AD neurodegeneration in cognitively normal elderly, the group that could profit the most from sleep preventive strategies.

The prevalence of both Alzheimer's Disease (AD) and stroke doubles each decade over 65 years old. Both are major causes of dementia, currently estimated to affect 46 million people worldwide. The current costs globally are $818 billion. Additionally, in population studies elders over 65 years, "covert" cerebral small vessel disease appears on MRI scans as silent lacunar infarcts in 25% as Microbleeds in 10%, and as focal or diffuse 'incidental' white matter disease (WMD) in 95%. WMD is extensive in 20%, with a clinical threshold effect around 10cc2. Small vessel disease is even more common in dementia, often coexisting with AD and independently contributing to cognitive decline and progression to dementia. Longitudinal imaging using cerebral amyloid labeling opens a new opportunity to understand the additive/interactive effects of small vessel disease and AD. The design of this study includes recruitment of two cohorts, including Mild Cognitive Impairment (MCI) and/or early Alzheimer Disease subjects from memory clinics and subjects with strokes/TIA from stroke prevention clinics. Inclusion criteria include the presence of moderate/extensive white matter disease, eg. Fazekas score of 2 (with confluent peri-ventricular hyperintensities) or Fazekas score of 3, as determined by previous MR or CT, > 60 years of age, Mini-Mental Status Exam (MMSE) scores ≥ 20. Subjects will undergo 3T structural MRI (including T1, PD/T2, FLAIR, GRE, DTI, ASL, and resting state fMRI), glucose PET, amyloid PET (using AV-45 florbetapir) and neuropsychological testing, as well as blood sampling. Repeat MR and PET/CT imaging and neuropsychological testing will be conducted at 24 months. The follow up assessments can also be completed at either year 1 or year 3 or Year 4 depending on the availability of study participants. The imaging portion is designed to closely parallel the Alzheimer's Disease Neuroimaging Initiative (ADNI) in order to benefit from the availability of both cognitively normal controls (NC), MCI and Alzheimer's disease subjects with minimal WMD.