Alzheimer’s disease (AD) is a disease associated with the destruction of brain cells resulting in the decline of cognitive functioning, memory, and social skills. The most common cause of AD is aging. There are approximately 36 million people worldwide who suffer from Alzheimer’s. Since AD is common and not entirely understood, it is important to better understand the processes regulating AD progression in order to develop more targeted treatments and interventions that can delay or prevent the disease.
Something I didn’t realize about Alzheimer’s disease (AD), until we talked about it in our Neurochemistry capstone class this week is that insulin has a compelling role in the progression of the disease. Obviously AD is multifactorial, since things like hyperphosphorylated tau and AB plaques are other problematic contributors to the disease. But interestingly, several studies have shown that overactivation of the P13-k/Akt/ mTOR signaling pathway is an early feature of AD.
Insulin is one of the key activators of this P13-k/Akt/ mTOR signaling pathway. While signaling through this pathway, it is crucial for the cell to maintain the proper activity level. Proper signaling through the P13-k/Akt/ mTOR signaling pathway allows for the beneficial processes resulting in DNA repair, cellular repair, translation of anti-stress proteins, and overall maintenance of healthy cell systems within the neurons of the brain.
Evidence is suggesting that insulin resistance is problematic occurrence within the neurons of people with AD. Insulin resistance does not allow the proper regulation of the P13-k/Akt/ mTOR signaling pathway because of sustained activation. This is a problem because insulin resistance in AD neurons has been associated with decreases in episodic and working memory, resulting in the symptoms of AD.
So how does this relate to diabetes? Well Type I Diabetes (T1D) is associated with hyperglycemia because the beta cells of the pancreas that produce insulin are destroyed by the person’s own body, resulting in decreased insulin action. Type II Diabetes (T2D) is associated with insulin resistance in peripheral tissues due to low insulin receptor expression and activity. Like T2D, AD can be associated with insulin resistance, but in this case confined to the neurons of the brain. In this way, AD could be considered Type III Diabetes. With this in mind, future research should consider treatments for AD that can minimize the impacts of insulin resistance in the brain.
Is Alzheimer’s Disease (AD) Type III Diabetes?
