Northwestern Researchers Label Alzheimer's Type 3 Diabetes

Researchers at Northwestern University in Chicago have announced that Alzheimer's disease could actually be a third form of diabetes.

According to the alumni magazine known simply as Northwestern, William Klein, professor of neurobiology and physiology, led the research team. A member of Northwestern's Cognitive Neurology and Alzheimer's Disease Center, he cited the findings as a brand new link between the fields of diabetes and Alzheimer's.

Previously, the medical community identified two types of diabetes. Patients with Type 1, also known as juvenile-onset diabetes, suffer from the body's lack of ability to manufacture insulin. Those with Type 2, which often develops much later in life than Type 1, experience either a deficiency of insulin or a resistance to it. They account for at least 90 percent of diabetes cases, according to the National Center for Chronic Disease Prevention and Health Promotion.

Insulin is a peptide hormone produced in the pancreas. Patients lacking sufficient levels in their bodies must either take oral forms of the hormone or inject themselves with it at regular intervals.

The Northwestern research was recently published in the Journal of the Federation of American Societies for Experimental Biology (FASEB). It explained why brain insulin signaling, which is essential for memory formation, stops functioning in Alzheimer's patients. According to the article, a toxic protein discovered in the brains of these patients removes insulin receptors from nerve cells. These cells, or neurons, are left resistant to insulin.

The protein identified by the researchers is amyloid beta-derived diffusible ligant (ADDL). It builds up in the brains of Alheimer's patients and has been shown to attack synapses that form memory. Prior research has demonstrated that individuals with Alzheimer's disease have lower levels of insulin in their brains than non-affected subjects do.

Both insulin and insulin receptors are essential to human learning and memory. Research suggests that once insulin binds to an insulin receptor in the brain, it unlocks a process required for neurons to survive and memories to be built.

The Northwestern team discovered that when ADDLs managed to bind to synapses, the process prevented insulin receptors from accumulating at the synapses wherever they were required. Their findings represent the first information on a molecular level to explain why nerve cells might become insulin-resistant for those suffering from Alzheimer's.

As a result of this study, medical researchers hope to be able to eventually determine the attributes of current drugs used to treat diabetes that might also help Alzheimer's patients. Their next goal is to discover how to make insulin receptors resistant to the onslaught of ADDLs.