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Browse 1,974 clinical trials for alzheimer's disease. Find studies that match your criteria and connect with research centers.
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NCT00001662
Glutamate is an amino acid released by brain cells that acts to excite other cells. Glutamate attaches to special sites on cells called AMPA (alpha-amino-2,3-dihydro-5 methyl 3-oxo-4-isoxazolepropanoic acid) receptors. The brain cells responsible for releasing glutamate are damaged in Alzheimer's disease and other conditions affecting thinking and reasoning. Researchers would like to see if giving patients a drug that attaches to AMPA receptors improves the symptoms of Alzheimer's disease. CX516 (Ampalex) is a test drug that affects the AMPA receptors. This study will investigate the effectiveness and safety of CX516 on patients with Alzheimer's disease. Patients will be given capsules of CX516 or placebo (sugar pill that neither harms nor helps) for up to 16 weeks in different amounts. The effectiveness of the drug will be measured by neurological tests. Safety will be monitored by frequent check-ups and lab examinations.
NCT00001323
The purpose of this study is to evaluate the cognitive processes of participants with schizophrenia, participants with nervous system and mental disorders, and healthy volunteers. Participants in this study will undergo cognitive tests of attention, memory, attention. Participants with attention deficit hyperactivity disorder (ADHD), traumatic brain injury (TBI), bipolar disorder, and Alzheimer's disease (AD) will be compared with participants with schizophrenia. A group of healthy adults and children will undergo cognitive tests to further delineate the degree of impairment in schizophrenia and neurological disorder participants.
NCT00004557
Patients with Alzheimer's disease (AD) perform poorly on tasks dependent on access to, and utilization of, previously acquired knowledge and skills. It has been commonly assumed that impaired knowledge in AD, as well as in other patients with cortical lesions, is due to an actual loss or disorganization of a specific knowledge base or system. This hypothesis has, however, recently been called into question by data from tasks that purport to tap knowledge on a more automatic and implicit level. For example, although AD patients are impaired on object naming and verbal fluency tasks, they show a normal pattern of semantic facilitation on reaction time based priming tasks. In fact, the level of facilitation or activation on these tasks has often been reported to be greater in AD patients than in normal individuals. These and similar data have been used to support arguments that performance decrements in AD patients are due to deficits in attentional and/or retrieval processes rather than a degradation of knowledge stores. The central focus of this project will be to test a model of the semantic representations of object that predicts increased facilitation or hyperpriming in AD patients as a result of degraded representations. The relationship between performance on on-line priming tasks, visual attention and spatial processes, and explicit and implicit measures of memory also will be examined. In addition to normal controls, patients with cognitive and memory impairments, but without semantically-based naming difficulties (elderly depressed, Huntington's disease, Korsakoff's disease) will serve as controls for overall slowness of response and degree of explicit memory deficit.