MUSC Discovers Link Between High Cholesterol and Alzheimer's Disease

19/10/06 A team of scientists at the Medical University of South Carolina (MUSC) has found evidence that further links high cholesterol levels to Alzheimer's disease. The research, led by MUSC neuroscientist, Narayan R. Bhat, Ph.D., further supports similar previous research as well as high cholesterol's role in inflammation which may trigger the disease. The findings were recently presented at the Society for Neuroscience annual meeting in Atlanta.

Bhat and his team of MUSC Neuroscientists tested their hypothesis that high cholesterol, resulting from either diet or genetic disposition, would intensify the brain's inflammatory response and spur amyloid generation that would, in turn, lead to the neurodegeneration and dementia characteristic of Alzheimer's disease.

A preliminary study of mice that were fed a high cholesterol, high fat diet for two months, and then tested on a memory task, showed a loss of working memory in association with a significant neuroinflammatory response. Parallel studies of mice with existing elevated cholesterol levels revealed similar signs of memory loss and neuroinflammatory responses regardless of the type of diet they were on.

These findings provide experimental evidence for the current idea that high cholesterol levels in the body resulting from dietary and/or genetic factors may contribute to the onset of cognitive decline associated with Alzheimer's disease. These findings could potentially pave the way for low-fat diets or, potentially, diets high in polyunsaturated fats as a preventive measure against the risk of developing Alzheimer's disease. In addition, an observed connection between diet-induced neuroinflammatory changes and memory deficit emphasizes the potential therapeutic usefulness of anti-inflammatory treatments against Alzheimer's-like dementia.

It is likely that high cholesterol levels may result in an inflammatory cascade as has been observed in cardiovascular disease, atherosclerosis. Potentially, systemic inflammation may also adversely affect tiny blood vessels in the brain, making them less effective at filtering out harmful compounds. The gathering of immune cells at site of inflammation in the brain could then initiate a cascade of events leading to the build-up of amyloid in the brain and synaptic/cognitive dysfunction.