Although a direct “yes” or “no” answer on whether there is a link between insulin levels and neurodegenerative diseases is desired, it is never that easy, because well… science. The further our knowledge extends on the brain and associated pathophysiology, the more we realize how interconnected and reliant certain systems and processes are on one another.
A third type of diabetes?
In the question of whether or not insulin is connected with Alzheimer’s, it is possible that the resistance to insulin within the brain is linked to this burdening disease. Insulin is more notably associated with the ever-rising diabetes. Type I and Type II diabetes are more commonly understood to be due to little or no pancreatic secretion of insulin and to peripheral insulin receptor resistance to insulin, respectively. Then there’s a Type III diabetes being proposed with a more common name, Alzheimer’s. Type III diabetes is hypothesized to be a result from central, instead of peripheral, resistance to insulin. Insulin is able to cross the blood-brain barrier (“BBB” a “safety border” between your blood circulating in your body and brain, protecting both from things not meant to be there) through passive diffusion and transcytosis in certain parts of the brain. Therefore, in type III, insulin is able to cross the BBB, but is resists binding to the receptors on the brain side.
How is insulin a bad guy? Irregularity in insulin signaling
I am focusing more on what is
called the
Forkhead box protein (FOXO) down at the bottom of the picture. What we want to have happen, is the FOXO gene to be functional, which leads to a cascade of transcriptions, resulting in longevity of neurons (what we want! Yay!), although too much FOXO can also be bad because too much of a good thing is a viable excuse here.. However, in the case of neuronal loss, insulin binds to the its respective receptor, a phosphorylation cascade happens, resulting in the inhibition of FOXO, therefore we don’t see the longevity of these neurons that we desire. We don’t want too much inhibition of FOXO, but we don’t want too much activation of it either, therefore its stubbornness to being regulated is what is burdensome. Once FOXO is inactivated (and subsequently removed from the nucleus), it has been shown to activate the POMC pathway – many more adverse impacts – uncaring of whether its actions are beneficial or not.
Curing age-related diseases
Although there is no set “cure” to neurodegenerative diseases like Alzheimer’s, there may be mechanisms with insulin involved (as a little glimpse is shown above). We can’t just shoot up patients with neurodegenerative diseases with insulin either, because it has an adverse effect throughout the whole body.
However, if you want to look into something hitting the forefront in neurochemistry, here is a cool link to a TED talk about Deep Brain Stimulation from a neurosurgeon, Andres Lozano. Although he talks more specifically about Parkinson’s disease, this treatment is starting to become more popular in medicine today and may be seen in the near future to activate the neurons we want activated for Alzheimer’s.
The Bigger Problem.. and a new cure?
I believe that one more TED talk is of necessity (and is shorter than the previous one…) Samuel Cohen speaks the bigger problem addressing Alzheimer’s (hint: lack of funding) and a HUGE breakthrough in the science realm where his laboratory is making recent breakthroughs.. You’ll have to watch.
A link between insulin and Alzheimer's and a breakthrough cure?
