As body fat increases, so do blood levels of a protein fragment linked to Alzheimer’s disease, a new study shows, which may begin to explain the recently reported association between obesity and the brain-wasting disease.

“We found that obesity by itself, even in otherwise healthy middle-aged people, is associated with elevated levels of the amyloid peptide that builds up and causes Alzheimer’s,” said Dr. Sam Gandy, director of the Farber Institute for Neurosciences in Philadelphia and one of the study’s authors.

“Amyloid is normally made all throughout the body at various lengths,” Gandy explained. “This particular form is believed to be the form that initiates build-up of amyloid plaques in the brain.”

Gandy, Dr. Ralph Martins at Edith Cowan University in Joondalup, Western Australia and their colleagues investigated whether levels of the peptide, plasma amyloid-beta 42,were related to body mass index (BMI) or fat mass in 18 healthy adults.

As BMI rose, so did amyloid-beta 42 blood levels, the researcher report in the Journal of Alzheimer’s Disease. The same was true for fat mass. But there was no relationship between BMI or fat mass and another peptide, amyloid-beta 40, which is not associated with disease.

Obesity-linked conditions like diabetes and heart disease may also increase Alzheimer’s risk, but when Gandy and his team adjusted the data for levels of insulin, cholesterol, and inflammation in an attempt to account for their influence, the fat-amyloid-beta 42 relationship remained. This suggests, Gandy said, that it’s the fat itself - not the diseases that excess weight can cause - that may be increasing levels of the dangerous protein.

“The amyloid beta is very attracted to fat,” he noted. “It might make sense that having a lot of lipids around would increase your tendency to hang on to a lot of amyloid beta rather than metabolizing it.” The potentially harmful protein could be stored up in body fat the same way that fat-soluble drugs and hormones are, he added.

The next step, Gandy said, will be to follow participants in the current study to see if any subjects develop Alzheimer’s disease and to investigate potential mechanisms for the fat-amyloid-beta-42 in the laboratory.

SOURCE: Journal of Alzheimer’s Disease, December 2005.