This week we discussed a topic that was completely new to me, Type III diabetes. According to “Possible implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis,” Type 2 diabetes (T2D) is a significant risk factor for developing Alzheimer’s disease (AD). One of the key features of T2D is resistance to insulin-either the insulin receptors in the body do not respond to the insulin produced by the pancreas or there isn’t enough insulin produced. Insulin is an important regulatory molecule because it controls how much glucose enters the cells of the body and remains the blood. Glucose is an important energy source that cells use to create new molecules, transport molecules in and out of the cell, and store energy. Patients with Type 2 diabetes do not use insulin appropriately to reduce the blood sugar levels, which leads to hyperglycemia.
Hyperglycemia and insulin resistance are problematic body wide but particularly in the brain. Hyperglycemia causes the body to use more insulin, which leaves less insulin available for use in the brain. Insulin plays several important roles in the brain. First, low levels of insulin leads to increased brain glucose metabolism. Increased brain glucose metabolism changes the process of memory and cognition. Lack of insulin decreases the release of the signaling chemicals in the brain, neurotransmitters, which are responsible for cognition and memory. Amnesia can result from decreased neurotransmitter release. Also, insulin resistance has been found to down-regulate b-amyloid-derived-diffusible ligands (ADDL) binding sites in the brain. This causes the brain to hyperphosphorylate Tau proteins. This is a fancy way of saying that the brain activates proteins that are the hallmark of Alzheimer’s disease. Once the Tau proteins are phosphorylated and begin to accumulate as neurofibrillary tangles, the brain struggles to break down the proteins and get rid of them. Tau protein phosphorylation leads to oxidative stress. Oxidative stress is hard on neurons and causes neurons to stop communicating with each other. Eventually, the neurons die and contribute to the pathogenesis of Alzheimer’s disease. Theses are only a few of the effects that insulin may have in the brain. Insulin controls inflammatory responses in the brain as well. This is another reason that insulin is thought to contribute to the development of AD disease.
According to the Center for Disease Control and Prevention, as many as 1 in 3 U.S. adults could have T2D by 2050 if steps are not taken to reduce risk factors for this disease. This is an increase from the current estimation of 1 in 10 U.S. adults living with diabetes. These statistics do not reflect the increasing number of children that are developing type 2 diabetes, as a result of the increase of childhood obesity. Similarly, the Alzheimer’s association predicts that the prevalence of AD will triple to 13.8 people by 2050. With prevalence of both diseases on the rise, this should be a call for action. It should also give people hope that there is a realistic means to reduce an individual’s risk of developing AD. By eating healthy, exercising regularly, maintain proper sleep habits and other healthy lifestyle changes, an individual can significantly reduce their risk of T2D and AD. It is important to spread the word because choices made now can affect a person today and tomorrow. Living right is only half the fight!
A Whole New Type of Diabetes
