Washington, May 1 : Scientists at the Salk Institute for Biological Studies say that they have probably unearthed the reason as to why diabetic individuals have a significantly higher risk of developing Alzheimer's disease.
The researchers say that experiments on mice have shown that the blood vessels in the brain of young diabetic animals are damaged by the interaction of elevated blood glucose levels and low levels of beta amyloid, a peptide that clumps to form the senile plaques that riddle the brains of Alzheimer's patients.
Lead researcher David R. Schubert, professor in the Cellular Neurobiology Laboratory, said that though the damage took place long before the first plaques appeared, the mice suffered from significant memory loss and an increase in inflammation in the brain.
"Although the toxic beta amyloid peptide was first isolated from the brain blood vessels of Alzheimer's patients, the contribution of pathological changes in brain vascular tissue to the disease has not been well studied," he said.
"Our data clearly describe a biochemical mechanism to explain the epidemiology, and identify targets for drug development," he added.
Past research had found diabetic people to be 30 to 65 per cent more susceptible to Alzheimer's disease than their non-diabetics counterparts. The risk was found to be associated with both type 1 and type 2 diabetes, which share hyperglycemia as a common pathogenic factor.
"Many studies have focused on altered insulin signaling in the brain as a possible mechanism for the association between Alzheimer's disease and diabetes but researchers paid much less attention to the direct affects of increased blood glucose levels on brain function and the pathogenesis of Alzheimer's," said lead author Joseph R. Burdo, a former postdoctoral researchers in Schubert's lab and now an assistant professor at Bridgewater State College in Bridgewater, Massachusetts.
In the current study, the researchers induced diabetes in young mice, whose genetic background predisposed them to acquire the symptoms of Alzheimer's with old age.
They observed that the mice suffered damage to blood vessels well before any overt signs of Alzheimer's disease-like nerve cell death or the acquisition of amyloid deposits, the hallmark of the disease-could be detected in their brains.
They also noted that the vascular damage was due to the overproduction of free radicals, resulting in oxidative damage to the cells lining the brain's blood vessels.
"While all people have a low level of amyloid circulating in their blood, in diabetics there may be a synergistic toxicity between the amyloid and high level of blood glucose that is leading to the problems with proper blood vessel formation," said Burdo.
The study has been published in the online issue of Neurobiology of Aging.