PRESS RELEASE
Accera Researchers Demonstrate that a Low-Carbohydrate, High-Fat Diet Reduced Markers of Alzheimer's Disease in a Transgenic Mouse Model
-Research with implications for Alzheimer's disease is published in Nutrition and Metabolism.
Broomfield, CO, October 17, 2005 - Accera, Inc. announced today that company researchers have demonstrated that an extremely low-carbohydrate, high-fat diet, known as a "ketogenic diet" reduced levels of the amyloid beta peptide in a transgenic mouse model of Alzheimer's disease (AD).
Amyloid beta (Ab) is a small protein that accumulates in the brains of people afflicted with AD and is a major target of drugs in development to treat AD. Previous research had implicated high-fat, high-cholesterol diets as playing a role in AD. Rodent studies had suggested that lipid rich diets increased the amount and deposition of Ab. However, the earlier work did not examine a high fat diet in combination with low carbohydrate intake. Accera's study demonstrated that high-fat diets alone did not increase Ab levels and other factors such as the carbohydrate content and total calories must be considered.
The paper titled "A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer�s disease" was published today in the open access journal, Nutrition and Metabolism (http://www.nutritionandmetabolism.com/). The work was done in collaboration with reMynd NV, a Belgian biotechnology company specializing in the testing of drugs for Alzheimer's disease. The study used transgenic mice developed at reMynd that express the "London" form of the Amyloid Precursor Protein (APP). Humans carrying the "London" form of APP invariably develop early onset AD. The transgenic mice develop pathology and behavioral deficits similar to those seen in human AD. These mice produce soluble levels of Ab as early as 3 months of age and exhibit extensive plaque deposition by 12 months. The mice also exhibit early behavioral deficits. In the Accera study, three month old mice were fed either a standard diet (SD) consisting of a high-carbohydrate, low-fat chow, or a ketogenic diet (KD) consisting of an extremely low-carbohydrate (>1%), high-fat chow (80%) for 43 days. At the conclusion of the experiment mice fed the KD were found to have 25% less Ab present in their brains when compared to the mice fed the SD. The diet also caused a 25% decrease in the more toxic form of Ab known as Ab42.
Samuel Henderson, Ph.D., Director of Research at Accera commented, "This work suggests that key aspects of Alzheimer's disease may be altered by metabolic intervention. The results add further support to our therapeutic approach for AD and will aid our drug development program." Accera is currently conducting a clinical trial with its first-in-class therapeutic, KetasynTM (AC-1202), for AD.
Richard Feinman, editor of the journal, highlighted the importance of the interaction of dietary components. He commented, "You might say that fat is the bomb, but insulin (from carbohydrate) is the fuse. Most studies of the deleterious effects of fat have been done in the presence of high carbohydrate. If carbs are low, dietary fat is oxidized rather than turned to body fat and possibly low carbs also limit amyloid beta production". Dr. Feinman, authored an accompanying editorial titled "When is a high-fat diet, not a high-fat diet."
About Alzheimer's disease
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the most common form of dementia in the elderly, affecting more than four million people in the United States today. The symptoms of AD normally begin with difficulty with memory and judgment, and eventually progress to impaired motor function. Currently, there are no cures for AD, and existing treatments are only minimally effective. AD presents a major health problem due to its enormous impact on individuals, families, the health care system, and society as a whole.
###