Researchers from Tulane University have published data linking high blood glucose to increasing toxicity of the beta-amyloid plaques that are characteristic of Alzheimer’s disease. Overproduction and accumulation of beta-amyloid protein can contribute to the neurofibrillary tangles in the brain that can cause Alzheimer’s. Research also suggests that blood vessels in the brain that become damaged also contribute to the disease. Now researchers have linked high blood glucose to the damaged cerebral blood vessels as a contributing factor.
The experiments, conducted in rats, used cell cultures from the linings of cerebral blood vessels in normal rats and those with long-standing diabetes. By exposing these cultures to high amounts of glucose without beta-amyloid, no changes in viability was observed in the cells. However, by exposing them to high glucose and beta-amyloid, the cell viability decreased by about 40%. Diabetic mice cells were more susceptible to this decrease in cell viability and cell death. This was true also in the presence of beta-amyloid with normal glucose levels.
- Recent research has highlighted the effects of blood vessel damage in the brain on Alzheimer’s disease.
- Rodent studies indicate that damaged blood vessels subjected to high blood glucose and beta-amyloid protein showed decreased cell viability and worsened Alzheimer’s.
- Diabetic rodents’ blood vessels were at greater susceptibility to damage and death due to beta-amyloid even in the presence of normal blood glucose levels.
Journal of Alzheimer’s Disease, October 2013