High blood sugar associated with prediabetes may increase the risk for Alzheimer's disease, a new study suggests.
Researchers found that insulin resistance -- higher-than-normal levels of blood sugar that often precede type 2 diabetes -- was related to poorer performance on memory tests taken by late-middle-age adults.
"The findings are interesting because people with diabetes are at increased risk for developing Alzheimer's disease, but we are only now learning why they may be at increased risk," said lead researcher Barbara Bendlin, an assistant professor of medicine at the University of Wisconsin-Madison.
The study results suggest that insulin resistance could increase the risk for Alzheimer's disease by altering the way the brain uses sugar (glucose), which is its primary fuel, she said.
However, "by altering insulin resistance in midlife, it may be possible to reduce future risk of Alzheimer's disease," Bendlin said. Medications and a healthy lifestyle are possible ways to do that, she said.
According to the American Diabetes Association, 29.1 million Americans have diabetes, and more than half of adults older than 64 have prediabetes. Poor diet, obesity and sedentary lifestyles are associated with insulin resistance, Bendlin noted.
"Healthier lifestyles may contribute to healthier brain aging by reducing insulin resistance," Bendlin said.
One expert cautioned that having prediabetes, or insulin resistance, doesn't mean you're doomed to develop Alzheimer's, the most common form of dementia.
This study shows that insulin resistance may make mental functioning worse and may be linked to reduced use of insulin in areas of the brain associated with Alzheimer's disease, but this does not mean that insulin resistance leads to Alzheimer's, said Dr. Luca Giliberto, an investigator at the Litwin-Zucker Research Center for the Study of Alzheimer's Disease at the Feinstein Institute for Medical Research in Manhasset, N.Y.
"We do not know what causes Alzheimer's disease," said Giliberto, who was not involved in the study. "We don't know if lowering blood sugar will prevent Alzheimer's."
For the study, Bendlin's team gave memory tests to 150 adults with no mental impairments, at average age of 61. The researchers also measured insulin resistance and had the participants undergo a PET brain scan.
More than two-thirds of the participants had a parent who suffered from Alzheimer's, about 40 percent had a gene mutation associated with increased Alzheimer's risk and roughly 5 percent had type 2 diabetes, according to the study.
The researchers found insulin resistance was associated with poorer processing of sugar throughout the brain. Worse performance in immediate memory was linked to lower sugar metabolism in the left medial temporal lobe, the authors said.
The report was published July 27 online in JAMA Neurology.
Dr. Sam Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York City, said it appears there may be a difference "between the dementia related to full-blown diabetes, which seems to be primarily dementia caused by hardening of the arteries in the brain, and the mental impact of insulin resistance, which some investigators believe is associated with Alzheimer's."
In the brain, insulin helps transmit messages between cells, he noted.
"We have long thought of Alzheimer's as a disease of defective brain signaling," said Gandy, who had no role in the study. "Conceivably, there is also a disease of defective insulin signaling, which this paper would support."
If that's true, Gandy added, "then efforts at sensitizing the brain to insulin, using drugs such as pioglitazone [Actos, a diabetes drug], would make sense and might well lead to slowing of degeneration."
Giliberto recommended healthy living as the best way to keep blood sugar under control and perhaps protect mental health.
"Increasing our health by reducing fats, reducing sugar, improving insulin resistance may reduce the risk of other factors, such as diabetes, on the susceptibility to Alzheimer's disease and mental decline," Giliberto said.