Researchers observing the effects of various diets on the brains of genetically engineered mice bred for studying Alzheimer’s disease found quite unexpectedly that mice fed a high protein, low carbohydrate diet, developed brains that were five per cent lighter than those of mice fed other diets.
The study was the work of lead author, Sam Gandy, a professor at The Mount Sinai School of Medicine in New York City and a neurologist at the James J Peters Veterans Affairs Medical Center in the Bronx NY, and colleagues from research centers in the US, Canada, Australia and the UK. The study is published this week in BioMed Central’s open access journal Molecular Neurodegeneration.
Many other studies have already suggested that low calorie, low fat diets rich in vegetables, fruits, and fish may delay or slow down Alzheimer’s disease, so Gandy and colleagues decided to take this a step further and compare the effects of several different diets on mice that were genetically engineered to have some of the disease characteristics of Alzheimer’s.
Alzheimer’s is a brain-wasting disease where the cerebral cortex shrinks, and microscopic beta-amyloid plaques form around neurons or brain cells and neurofibrillary tangles form inside them.
Beta amyloid is a protein fragment snipped from an amyloid precursor protein (APP), whose role in the brain is not fully understood. What we do know is that in a healthy brain, beta amyloid fragments are broken down and eliminated, but in Alzheimer’s disease, they build up and form hard, insoluble plaques.
For the study, Gandy and colleagues tested four different diets on mice that were genetically engineered to express a mutant form of APP.
For 14 weeks (from the age of 4 weeks until 18 weeks) they fed the male and female mice on one of four diets: (1) a regular (reference) diet; (2) a high fat/low carbohydrate diet (60 per cent fat, 30 per cent protein, 10 per cent carbs, by calorie value); (3) a high protein/low carbohydrate diet (60 per cent protein, 30 per cent fat, 10 per cent carbohydrate by calorie value); or (4) a high carbohydrate/low fat diet (60 per cent carbohydrate, 30 per cent protein, 10 per cent fat, by calorie value).
After this, the researchers did post mortems on the brains of the 18-week old mice and measured their weight, plaque build up and structural differences in those regions known to be involved in the memory defects of Alzheimer’s disease (eg the hippocampus).
To their surprise, they found that the brains of the mice that had been fed the high protein/low carbohydrate diet were five per cent lighter than those of mice on the other diets, and regions of the hippocampus were less developed.
However, until they test for this effect in non-genetically engineered mice, it remains unclear whether the loss of brain mass is linked to the type of plaque found in Alzheimer’s disease.
Meanwhile, since previous studies have already indicated that diet may play a role in the progress of Alzheimer’s, the researchers tentatively put forward the theory that perhaps a diet high in protein makes neurons more vulnerable to the type of plaque that is characteristic of Alzheimer’s.
To support this theory they pointed out that the mice that were fed on a high fat diet had higher levels of plaque proteins in their brains but this did not raise the amount of plaque.
Gandy told the media that:
“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 [Alzheimer’s Disease].”
The only way to verify this would be to do prospective randomized double blind diet trials, he said, explaining that while this would be difficult, it would be worth it if “there is a real chance that the ravages of AD might be slowed or avoided through healthy eating”. “Such trials will be required if scientists are ever to make specific recommendations about dietary risks for AD,” he added.
“Dietary composition modulates brain mass and amyloid beta levels in a mouse model of aggressive Alzheimer’s amyloid pathology.”
Steve Pedrini, Carlos Thomas, Hannah Brautigam, James Schmeidler, Lap Ho, Paul Fraser, David Westaway, Peter Hyslop, Ralph Martins, Joseph Buxbaum, Giulio Pasinetti, Dara Dickstein, Patrick Hof, Michelle Ehrlich and Sam Gandy.
Molecular Neurodegeneration, 2009, 4:40 (21 October 2009).
Source: BioMed Central, Alzheimer’s Health Assistance Foundation.
Written by: Catharine Paddock, PhD