A research team from the US, Canada, and the UK tested four differing menus on transgenic mouse model of AD, which express a mutant form of the human amyloid precursor protein (APP). APP's role in the brain is not fully understood; however it is of great interest to AD researchers because the body uses it to generate the amyloid plaques typical of Alzheimer's.
These mice were fed either (1) a regular diet, (2) a high fat/low carbohydrate custom diet, (3) a high protein/low carb version or (4) a high carbohydrate/low fat option. The researchers then looked at the brain and body weight of the mice, as well as plaque build up and differences in the structure of several brain regions that are involved in the memory defect underlying AD.
Unexpectedly, mice fed a high protein/low carbohydrate diet had brains five percent lighter that all the others, and regions of their hippocampus were less developed. This result was a surprise, and, until researchers test this effect on non-transgenic mice, it is unclear whether the loss of brain mass is associated with AD-type plaque. But some studies in the published literature led the researchers to put forward a tentative theory that a high protein diet may leave neurons more vulnerable to AD plaque. Mice on a high fat diet had raised levels of plaque proteins, but this had no effect on plaque burden.
Aside from transgenic mice, the pressing question is whether these data have implications for the human brain. "Given the previously reported association of high protein diet with aging-related neurotoxicity, one wonders whether particular diets, if ingested at particular ages, might increase susceptibility to incidence or progression of AD," says Sam Gandy, a professor at The Mount Sinai School of Medicine in New York City. The only way to know for sure would require prospective randomised double blind clinical diet trials.
MEDICA.de; Source: The Mount Sinai School of Medicine in New York City