This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Amyloid plaque in the brain is evident in the neuropathology of AD. The manipulation of the making and accumulating of this amyloid is one of the most proposed mechanisms in the intervention of AD. There are studies that have shown the link between cholesterol and AD and that the decreasing of the cholesterol levels may then change the processing of the amyloid which in turn would decrease the levels of A beta production decreasing plaque formation. There have been studies to show the association between dietary cholesterol and biological markers for AD where high cholesterol diets in mice increase A beta production. The studies support the notion that circulating cholesterol may be a risk factor for increasing A beta production. There is also some data show that differences in cholesterol levels also affect cognitive function. The studies indicate that elevated cholesterol levels may be related to amyloid deposits and cognitive function and that lowering the cholesterol may lead to cognitive benefit. Simvistatin was chosen due to its ability to cross blood brain barrier, has a good safety profile and it is the second most commonly used agent.
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