14 DAY TRIAL // Researchers at Rhode Island Hospital and Brown Medical School have discovered that insulin and its receptors drop significantly in the brain during the early stages of Alzheimer's disease, and that levels decline progressively as the disease becomes more severe.
This result comes to support the theory which says that Alzheimer's is a new type of diabetes. In addition, they've also found that acetylcholine deficiency, a hallmark of the disease, is linked directly to the loss of insulin and insulin-like growth factor function in the brain.
"Insulin disappears early and dramatically in Alzheimer's disease. And many of the unexplained features of Alzheimer's, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes," says senior author Suzanne M. de la Monte, a neuropathologist at Rhode Island Hospital and a professor of pathology at Brown Medical School in Providence, RI.
The study analyzed postmortem brain tissue of 45 patients with a diagnosis of either normal aging or different degrees of Alzheimer's neurodegeneration.
Researchers analyzed insulin and insulin receptor function in the frontal cortex, a major area affected by Alzheimer's. They found that with increasing severity of the disease, levels of insulin receptors and the brain's ability to respond to insulin decreased markedly.
"In the most advanced stage of Alzheimer's, insulin receptors were nearly 80 percent lower than in a normal brain," de la Monte says.
Researchers found two parallel abnormalities related to insulin in Alzheimer's. First, insulin levels decline as the disease progresses. Second, insulin and its related protein IGF-I lose their ability to bind to corresponding cell receptors, creating a resistance to the growth factors and thus causing cells to malfunction and eventually die.
"This has important implications for treatment," de la Monte says. "If you could target the disease early, you could prevent the further loss of neurons. But you would have to target not just the loss of insulin but the resistance of its receptors in the brain."