Diabetes and insulin resistance linked to Alzheimer’s

Individuals with type 2 diabetes or insulin resistance have a higher risk of developing Alzheimer’s disease because they are more likely to develop plaques in the brain associated with Azheimer’s, says a report published in the medical journal, Neurology.

The study consisted of 135 participants, all from Hisayama, Japan. Their average age was 67 years.

Participants underwent a range of diabetes glucose tests to measure their blood glucose levels. The researchers monitored them for Alzheimer’s disease symptoms for the subsequent 10 to 15 years. Approximately 16% of them developed Alzheimer’s disease.

After death, the investigators examined their brains for plaques or tangles – physical signs of Alzheimer’s disease. Only 16% had had symptoms of Alzheimer’s disease before death. However, 65% of the people who died had plaques.

The researchers discovered that those who had abnormal results on three blood sugar control tests were considerably more likely to develop plaques.

“Further studies are needed to determine if insulin resistance is a cause of the development of these plaques. It’s possible that by controlling or preventing diabetes, we might also be helping to prevent Alzheimer’s disease,” said study author Dr Kensuke Sasaki from Kyushu University in Fukuoka, Japan.

In separate research involving cases of rheumatoid arthritis, the protein produced appears to protect sufferers against the development of Alzheimer’s disease.

Tests on mice with memory loss showed those given the protein fared better in tests according to a study published in the Journal of Alzheimer’s Research. A synthetic version of GM-CSF protein is already used as a cancer treatment.

It had already been recognised that people with rheumatoid arthritis were less likely to develop Alzheimer’s, but the protective link was thought to be linked to non-steroidal anti-inflammatory drugs (NSAIDs) taken by people with the condition.

Rheumatoid arthritis sufferers’ immune system produces attacking proteins – including GM-CSF. 

The research team from the University of South Florida found the Alzheimer’s mice treated with GM-CSF fared substantially better on tests measuring memory and learning, and performed at a similar level to mice of the same age without the condition.

Even the healthy mice treated with GM-CSF performed slightly better than their untreated peers. Those that received the placebo continued to do poorly.

“Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer’s disease,” said lead researcher Dr Huntington Potter in a BBC News report.

An artificial version of GM-CSF, a drug called Leukine, is already approved by the United States Food and Drug Administration and has been used to treat cancer patients who need to generate more immune cells.

“Our study, along with the drug’s track record for safety, suggests Leukine should be tested in humans as a potential treatment for Alzheimer’s disease,” said Dr Potter.

British experts said the American study was “an important first step” and tests were needed to see if the drug worked for people with Alzheimer’s.