Return to Main Menu

Researchers: high cholesterol linked to Alzheimer’s by Tim Gehret Public Relations A team of MUSC scientists found evidence that further links high cholesterol levels to Alzheimer’s disease. The research, led by MUSC neuroscientist Narayan R. Bhat, Ph.D., supports previous research of 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, Ga.   Previous studies linked memory loss to subjects genetically disposed to high cholesterol, Bhat said. However, Bhat and his team of MUSC neuroscientists wanted to test their hypothesis that high cholesterol, resulting from either genetic disposition or diet, 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 fed. 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.   “Implicit in these findings is a new hope for low-fat diets or, potentially, diets high in polyunsaturated fats as a preventive measure against the risk of developing Alzheimer’s disease,” Bhat said. “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 observed in the 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.     Friday, Nov. 10, 2006 Catalyst Online is published weekly, updated as needed and improved from time to time by the MUSC Office of Public Relations for the faculty, employees and students of the Medical University of South Carolina. Catalyst Online editor, Kim Draughn, can be reached at 792-4107 or by email, catalyst@musc.edu. Editorial copy can be submitted to Catalyst Online and to The Catalyst in print by fax, 792-6723, or by email to catalyst@musc.edu. To place an ad in The Catalyst hardcopy, call Island Publications at 849-1778, ext. 201.