In a study on animal models, lead author Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, utilized chronic high fat diets to cause a two-fold increase in mean body weight.
In these models, there was a marginally reduced mean brain weight and a significantly reduced mean brain weight/body weight ratio, providing evidence that obesity with T2DM is sufficient to cause mild global atrophy in the brain.
"In essence, the brain shrinks and several biochemical and molecular abnormalities found in patients with AD, including brain insulin resistance, develop with chronic obesity and T2DM. However, the extent of the abnormalities in no way matches AD," De la Monte said.
Researchers found that the neuropathological abnormalities were mild and the associated brain insulin resistance could serve as a co-factor in the development and progression of AD.
Overall, the study showed that that the effects of obesity and T2DM can essentially aggravate or contribute to the severity or progression of AD, but cannot be the sole cause of the condition.
The findings suggest that strategies to reduce obesity and prevent or control T2DM could modify the clinical course of mild cognitive impairment and AD.
"We don't know yet if these effects of T2DM/obesity are reversible with weight loss. However, we're fairly sure that the abnormalities are related to the T2DM that accompanies obesity and not just increased weight," De la Monte said.
The study appeared in the Journal of Alzheimer's Disease.