HONG KONG (Reuters) - People with insulin resistance and type 2 diabetes are more likely to develop plaques in the brain associated with Alzheimer’s disease, researchers in Japan reported on Thursday.
The study involved 135 elderly participants in the town of Hisayama, Fukuoka prefecture, who had their blood sugar levels checked several times at the start of the study. They were then monitored for signs of Alzheimer’s disease for 10 to 15 years.
After they died, researchers conducted autopsies on their brains and found plaques, particularly in those who had high blood sugar levels while they were alive.
“It is possible that adequate control of diabetes in midlife may contribute to ... prevention of Alzheimer’s disease,” wrote lead researcher Kensuke Sasaki at Kyushu University in Fukuoka in an email reply to Reuters.
Prevalence of type 2 diabetes and Alzheimer’s disease are soaring around the world due to growing obesity and people living longer lives, but most healthcare systems are ill equipped to handle such chronic illnesses.
Twenty-one participants, or 16 percent, developed Alzheimer’s disease before they died and plaques were found in all of their brains. But the autopsies also found plaques in other participants who had abnormally high blood sugar levels.
Plaques were found in 72 percent of people with insulin resistance and 62 percent of those with no indication of insulin resistance, the researchers wrote.
“The point is that insulin resistance may possibly accelerate plaque pathology (development),” Sasaki wrote.
Insulin resistance is the stage before diabetes and it occurs when insulin, a hormone in the body, becomes less effective in lowering blood sugar.
A few studies in the past explored the relationship between diabetes and Alzheimer’s, but findings were inconsistent and it was never certain which was the cause and which the result.
But this study has the longest observation period so far and the researchers said it was more likely that insulin resistance or diabetes resulted in Alzheimer’s disease.
Reporting by Tan Ee Lyn; Editing by Ron Popeski