View clinical trials related to Cognitive Dysfunction.
Filter by:Individuals with type 2 diabetes have an increased risk of developing cognitive dysfunction followed by dementia in late life. Obesity, physical inactivity and "systemic low-grade inflammation" are strong risk factors and play a crucial role in this network of diseases. Brain-derived Neurotrophic factor (BDNF) is produced in brain as well as several tissues outside brain eg muscle cells. Low BDNF are associated with cognitive dysfuction, obesity and type 2 diabetes. The investigators include 200 individuals divided into three groups: 80 individuals with type 2 diabetes, 80 age and BMI-matched controls and 40 individuals with impaired glucose tolerance. The project will test the hypothesis, that low systemic BDNF are associated with accumulation of abdominal fat, cognitive dysfunction and insulin resistence with different effect in men and women.
The present study aims at combining biochemical methods with various types of imaging techniques to identify the pathophysiology of Alzheimer's disease (AD). The main interest is to find markers associated with the very early steps in the pathology of this disease. The investigators shall thus screen for i) molecules in cerebrospinal fluid (CSF) and plasma specific for AD, and ii) brain imaging markers (e.g. MRI and PET) that correlate to detailed clinical assessments. Biomarkers of interest would then be useful to: 1. Enable accurate detection of the disease early on. Such biomarkers need to specifically reflect the very early pathophysiology of AD and distinguish it from disorders with similar symptomatology, such as other types of dementia and major depression. The sensitivity and specificity of these biomarkers in combination with clinical assessment should be of at least 90%. 2. Enable prediction of the course of events of the disease, such as the disease rate in individual patients. Biomarkers that can predict the pattern of future symptoms will be extremely valuable. 3. Allow monitoring of early effects of new disease-modifying therapies (so-called surrogate biomarkers). Currently clinical therapeutic trials for AD require large patient groups together with long-term treatment. Both size of the groups and treatment time will be reduced with the help of surrogate biomarkers. 4. Study the pathogenesis of the disease. Biomarkers can be used to investigate in detail early alterations in AD patients. For instance, changes in the levels of certain molecules in CSF together with genetic predisposition could then be correlated to clinical signs and changes detectable by brain imaging. This can lead to identification of new therapeutic targets that could easily be monitored in future trials.
There is substantial research on the effects of physical exercise on cognitive functions. However, less attention has been paid on the requirements of training intensity and length to enhance cognitive abilities in the elderly. To the investigators knowledge no studies have evaluated the effects of extensive endurance exercise training on cognitive functions by studying elderly marathon runners and bicyclists. On the basis of the scientific literature published so far it is not known whether the beneficial impact of endurance exercise training depends on the intensity of training. The investigators therefore designed a cohort study with adequate power in order to evaluate the effects of intensive endurance exercise training on cognition. This trial, an Austrian prospective cohort study in cognitive function of elderly marathon-runners (APSOEM) is being conducted and will compare neuropsychological performance outcomes of elderly marathon runners or bicyclists with controls matched concerning age, education years, occupation, and verbal intelligence.
This multi-center (6 sites: Helsinki, Kuopio, Oulu, Seinäjoki, Turku, Vantaa) intervention study aims to prevent cognitive impairment, dementia and disability in 60-77 year old persons at an increased dementia risk. The 2-year multi-domain life-style intervention includes nutritional guidance, exercise, cognitive training, increased social activity, and intensive monitoring and management of metabolic and vascular risk factors. The primary outcome is cognitive impairment measured by a sensitive Neuropsychological Test Battery (NTB), and Stroop and Trail Making tests to capture early cognitive impairment typical for both Alzheimer's disease and vascular dementia. We hypothesize that the multi-domain intervention will reduce cognitive impairment in the study group compared to the control group during the initial 2-year intervention period and reduce dementia incidence after the extended follow-up (until at least 300 participants have developed dementia).
ICU-acquired weakness represents a common and often devastating disease process which affects greater than 50% of critically ill patients. This pathogenesis of this acquired disease is multifactorial and results in variable severity, ranging from mild, transient to severe, permanent dysfunction of peripheral nerves in additional to muscle. In affected patients, weakness may persist for months to years after the acute phase of their illness, and has been implicated as a major contributor to decreased functional status and quality of life. Muscle ultrasound has been validated for assessment of muscle size as well as diagnosis of myopathic and neuropathic changes in patients with other known neuromuscular diseases. The use of muscle ultrasound or other imaging modalities for diagnosis or monitoring of ICU-acquired weakness has not been studied, although a single study using muscle ultrasound has shown significant change in muscle size in ICU patients receiving high dose corticosteroids and a prolonged course of paralytic agents. The investigators plan to use multiple modalities to examine skeletal muscle catabolism, function, and structure in patients during critical illness and recovery. The investigators will combine physical exam, hand grip dynamometry, electrophysiologic studies, serum biomarkers, muscle biopsies, and muscle ultrasound to assess a group of critically ill patients during their hospital stay. The investigators will obtain additional data, including neuropsychiatric assessments, severity of illness scores, administration of potentially harmful medications, and pertinent daily laboratory data. This study will last approximately 12 months.
Probands with MCI are at high risk to develop Alzheimer´s dementia (AD). Simvastatin may lower the production of Amyloid, a hallmark of AD in the brain. The primary hypothesis of the study is that 60 mg Simvastatin significantly reduces the Clinical Dementia Rating -Sum of boxes (CDR-SOB) in individuals with MCI as compared to MCI receiving placebo or 20 mg Simvastatin