Active clinical trials for "Alzheimer Disease"

This is a three-year study to determine if estrogens can prevent memory loss and Alzheimer's disease in women with a family history of Alzheimer's disease.

The overall goal of this imaging trial is to evaluate [18F]PI-2620, a tau targeted positron emission computed tomography radioligand, in individuals with tauopathies and healthy volunteers (HV).

This study is being done to learn about inflammation in the brain of those with Alzheimer's disease (AD). The purpose of this study is to determine if 11C-ER176 is able to accurately measure inflammation in patients with Alzheimer's disease. Both patients (with either mild cognitive impairment (MCI) or Alzheimer's disease) and healthy controls (participants without memory complaints or impairment) will be included in this study.

Alzheimer's disease (AD) is the leading cause of dementia and its prevalence is estimated to exceed 100 million affects by 2050, becoming the main public health problem worldwide. Classically, AD has been considered a clinicopathological entity characterized by a progressive cognitive decline with early memory impairment followed by other cognitive domains, and an underlying neuropathological pattern characterized by extracellular accumulation of β-amyloid protein (Aβ) in the form of neuritic plaques, intracellular deposits of tau protein in the form of neuritic strands and neurofibrillary tangles, neuronal and synaptic loss and glial proliferation. In this context, a "probable" AD diagnosis was based on determining the presence of dementia and ruling out other potential aetiologies while a definite one required confirmation by post-mortem examination. In the last 15 to 25 years, progress in imaging and cerebrospinal fluid (CSF) biomarkers has enabled a change of the AD conceptualization from a clinical-pathological entity to a clinical-biological one. These new diagnostic criteria also divides the course of AD into 3 stages: (1) a preclinical phase, which would include persons with positive AD biomarkers and normal cognitive performance (the subjective perception of cognitive decline [SCD] is also part of this stage); (2) a phase of mild cognitive impairment (MCI), characterized by cognitive performance lower than expected by age and educational level; and (3) a dementia phase, once cognitive deficits interfere with the activities of daily living. This new conceptualization brings the opportunity of identifying the disease in very early symptomatic pre-dementia stages or even before symptoms appear, creating a window of opportunity for dementia prevention. The lack of positive results in the different clinical trials performed to date in patients with AD dementia has redirected the focus of therapeutic strategies towards preventing the development of dementia. For this reason, a detailed characterization of risk factors is of vital importance for identifying the persons who could benefit from a possible preventive strategy, as well as the optimal moment to carry out the intervention. A recent effort by the Lancet Commission on Dementia Prevention, Intervention, and Care reported the relative risk for incident dementia of the main modifiable risk factors (low education in early life; hypertension, obesity, and hearing loss in midlife; smoking, depression, physical inactivity, social isolation, and diabetes in late life). In addition, the Framingham Heart Study has shown that age, marital status, BMI, stroke, diabetes, ischemic attacks, and cancer are independent predictors of event risk in the final multivariate model and were used to construct a risk algorithm. These set of risk factors associated with an increased risk of incident dementia can be coupled with well-known genetic risk factors such as APOE genotype and with the presence of very mild symptoms, like self-perception of cognitive decline to create individual estimates of risk for dementia, taking also into account the presence of cognitive decline or impairment. The possibility of creating individual estimates of risk of dementia implies a personalised medicine approach and results in a change from the traditional diagnostic paradigm to a new one in which people at risk are attended in order to disclose risk factor estimates and offer them personalised solutions. This paradigm shift brings important consequences. On one hand, disclosing medical information may potentially generate emotional impact, psychological burden or harm. Although current experience with both disclosing APOE-e4 genetic status and amyloid status reveals that it is safe, one still needs to understand the potential risks and benefits of disclosing risk estimates for developing dementia. On the other hand, newly designed infrastructures that are focused in the assessment and follow-up of pre-dementia patients at high risk to develop dementia are needed, since they clearly represent a distinct population from the one attending dementia clinics. These "prevention infrastructures" would offer individual risk profiling accompanied by personalised risk reduction plans including, but not limited to, primary prevention advice and secondary prevention approaches (e.g. inclusion in prevention clinical trials). With the ultimate aim of assessing and understanding the value of these "dementia prevention infrastructures", several research questions need to be beforehand addressed such as the following: Is disclosing risk factor estimates safe from the emotional and psychological point of view? Is there any benefits derived from the personalised plans received by subjects? Would the creation of Dementia Prevention Clinics be cost efficient? The BBRC-DevPrev-2018 study aims at answering the questions stated above.

Alzheimer disease is a frequent disease in the late ages that results in global alteration of cognitive functions. In which memory complaint can be isolated in the early stages. Physiopathology of neuronal degenerescence in Alzheimer disease is complex, two main histological lesions are known, amyloid plaques and neurofibrillar tangles. Beyond the histological knowledge, alterations of neuronal metabolism are described such as oxydative phosphorylation and glycolytic pathway. These metabolism alterations are involved in neuronal death. Multi-nucleus magnetic resonance spectroscopy is a non-invasive non-irradiant imagery technique already used in routine. This technic allows the phosphoenergetic pool assessment, that inform about cellular metabolism. The aim of the study is to explore the phosphorylated metabolism patterns as predictive biomarkers of cognitive decline in patients with a memory complaint diagnosed.

This research was carried out with the objective of verifying the possibility of intervention through cognitive training protocols to assist in the stimulation of neurons and to delay the degradation resulting from Alzheimer's disease in its initial phase. The specific objective of this research was to develop and validate a virtual environment of games (called SorrisoTur) that allows the intervention of cognitive training.

The study will examine the impact on cognitive reserve of a pharmacist-physician patient-centered medication therapy management intervention to address inappropriate medication use as identified by the Beers 2015 list. By bolstering cognitive reserve, this project will directly address the National Alzheimer's Project Act 2015 priorities serving to delay onset of symptoms in preclinical dementia. The results of this study will provide valuable insights on how to expand this intervention to reduce the prevalence and associated healthcare costs of symptomatic Alzheimer's disease.

This study will obtain data from urine in subjects administered flortaucipir in an Avid-sponsored study to augment the calculation of radiation dosimetry estimates.

A Multicenter national longitudinal cohort study including at least 800 individuals consecutively recruited from French Research Memory Centers and followed-up over 24 month and included in Memento.

The study is designed to assess the demographic, clinical and imaging associations with the presence of microbleeds in atypical Alzheimer's disease. The primary hypothesis is that cognitive and functional performance will be poorer in atypical Alzheimer's subjects with microbleeds compared to those without microbleeds.