Deposits of a hormone called amylin in the brain may indicate risk for developing dementia and type 2 diabetes, according to a study published online in the Annals of Neurology. The analysis by researchers at the NIA-funded Alzheimer's Disease Center at the University of California, Davis, is the first to identify amylin deposits in post-mortem brain tissue from older people who had been diagnosed with Alzheimer's disease or vascular dementia and diabetes. The findings also indicated that amylin may play a similar role in the Alzheimer's disease process as amyloid protein, a hallmark of the disorder.
Amylin (also known as islet amyloid polypeptide) is a hormone expressed and secreted with insulin. It influences blood sugar levels; when too much is secreted, risk for developing diabetes increases. These new findings show that amylin deposits can also build up and form plaques in the brain, similar to amyloid plaques found in Alzheimer's disease.
The researchers examined post-mortem brain tissue from three groups of volunteers older than 70 years: those who had diabetes and dementia (vascular dementia or Alzheimer's), those who had Alzheimer's but no diabetes, and those free of these disorders. Investigators found significant amylin deposits in the brain tissue of people with both dementia and diabetes. Surprisingly, they also found amylin in people with Alzheimer's but without diabetes—perhaps because these individuals had undiagnosed insulin resistance. The healthy controls had few amylin deposits.
The study, led by Dr. Florin Despa, may explain why people with diabetes are at risk for dementia. Like amyloid, amylin circulates in the blood and, during the disease process, is overproduced and not cleared normally, building up in the brain. Over time, both proteins lead to the loss of brain cells and brain damage. Amylin buildup in the brain's blood vessels may also play a role in amyloid buildup and contribute to risk for Alzheimer's, the study found.
Jackson K, et al. Amylin deposition in the brain: A second amyloid in Alzheimer's disease? Annals of Neurology July 30, 2013