Does diet outweigh genetics when it comes to Alzheimer’s risk? microbiologystudy

Genes play a role in whether someone gets Alzheimer’s, but new research from Northeastern University psychology and bioengineering professor Craig Ferris found that diet may have a greater impact on whether someone gets this disease.

Ferris was part of a study published in BMC Neuroscience that looked at male and female rats, some of which had genes that can increase the risk for Alzheimer’s. The animals were put on high-fat, high-sugar diets to see which ones had the worst cardiovascular function by the end.

Despite females being at a higher risk for Alzheimer’s, the researchers found that male rats without a genetic risk for the disease showed the most deficits when it came to cognitive performance.

“We got the results and said ‘Wow, that’s not what we expected,'” Ferris said. “It was the normal guys eating McDonald’s that had all the problems.”

The 4-month-old rats were put on this diet for a span of four months and then tested for changes in cognitive behavior. During this time, the animals were fed a diet that was nearly half carbohydrates, with about 34% of those carbs being sucrose. The diet was also made up of 21% fat and 17% protein.

The rats used in the study were adults. Ferris said this was because aging is the most significant risk factor when it comes to Alzheimer’s disease, so studying adult animals gave a more clear picture of other risk factors like genetics and diets.

Researchers hypothesized that the female rats with the genetic risk factor for Alzheimer’s would show the greatest deficit on this diet, as women who carry this gene have a higher risk for early onset Alzheimer’s. This, plus the genes and diet, made them most likely to show deficiencies.

But this was not the case. Using a 3D MRI rat atlas, scientists took images of the rats’ brains and analyzed 173 different areas. It was the wild type male rats (the ones without the gene) that showed the most changes.

The imaging showed that these rats had enhanced connectivity in the neural circuits associated with food consumption and metabolism.

The male rats without the E4 gene for Alzheimer’s also showed cognitive deficits when it came to maze testing, as opposed to the female rats without this gene and the male and female rats with this gene.

The results, Ferris said, are not necessarily new: it’s been known that a poor diet can increase risk for disease. But what was surprising was what researchers found when imaging the rats’ brains.

These male rats in the control group also showed whole brain hyperconnectivity, especially in the hippocampus.

“One of the cool spin-outs from that whole story is that we started to analyze brain connectivity and how the brain was rewired in these guys and came up with a really exciting finding,” Ferris said.

“The functional connectivity to the cerebellum, of all things, was significantly altered. And it turns out that parts of the cerebellum control feeding. It really turned out to be understanding what we thought was disruption and feeding behavior for these animals. The males had disrupted feeding behavior based upon how they were rewired.”

The research builds on the theory that Alzheimer’s could be caused by a decrease in vascular activity.

“That’s probably really at the foundation of Alzheimer’s—slow disruption of blood to the brain barrier,” Ferris said.

“A lot of key areas at risk are areas like the midbrain dopaminergic system for Parkinson’s, the hippocampus for dementia and Alzheimer’s. Years ago, they said, ‘Wow, it’s all about amyloid beta and all of this junk that accumulates in your head.’ … That amyloid beta hypothesis has been jettisoned by the community. … The science is moving toward cardiovascular disease.”

This story is republished courtesy of Northeastern Global News news.northeastern.edu.