Active clinical trials for "Cognitive Dysfunction"

This study will investigate the performance of physician readers trained to read florbetapir-PET scans using electronic media training.

The study is designed to evaluate whether a florbetapir F 18 PET scan can impact clinical thinking when physicians are determining the likely cause of a subject's cognitive impairment.

The aim of the study is to investigate the feasibility of using a virtual supermarket as an intervention tool for overcoming deficits in executive function as well as enhancing IADL performance among persons with Mild Cognitive Impairment. The working hypotheses are that there will be improvement in executive functions, and the improvement in the executive functions will result in better performance in Instrumental Activities of Daily Living, both generally and especially in shopping task

This is a non-pharmacological study evaluating the feasibility of a neurofeedback training program in elderly with mild cognitive impairment (MCI) according to recruitment, retention, attendance, acceptability data.

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.

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.

Cognitive dysfunction is the impairment of mental process of perception. memory and information processing which allow the human to acquire knowledge and plan for the future. The etiology of Post operative cognitive dysfunction (POCD) is unclear and seems to be multifactorial involving a combination of patient, surgical, anesthetic and environmental factors. The definition of day surgery in Great Britain and Ireland is clear; the patient is admitted and discharged on the same day.

In the cross sectional study "Adelahyde 1" which took place between 2001 and 2005, the investigators data suggest that vascular alterations may play a role in the setting of subjective memory complaints. This longitudinal study (Adelahyde 2) aims to confirm the role of vascular factors in the evolution of cognitive function and dementia.

The purpose of this study is to compare different combinations of cognitive training in retired professional football players and military veterans with a history of repeated concussions and persistent symptoms of impaired memory, concentration, attention, focus, or thinking.

Post operative cognitive dysfunction (POCD) is a well-recognized complication of patients undergoing cardiac surgery. Previous studies reported near-infrared spectroscopy provides information on the occurrence of cerebral desaturation resulted in POCD. But evidence of POCD after general surgery has been lacking. Especially, the prone position is used primarily for surgical access to the posterior spine, if there is any significant lowering of the legs or tilt of the entire table, venous returns may be decrease or augmented accordingly. The purpose of this study was to examine the relationship between POCD and intra-operative cerebral oxygen saturation after spine surgery in elderly patients.