Many may wonder the rationale behind this title, and indeed it seems a strange connection to make. But the truth of Alzheimer’s disease lies in insulin receptors, and eventually insulin resistance. These receptors are, of course, localized to the brain, and not the pancreas (as in the case of diabetes as we know it). To understand the idea of Alzheimer’s as an insulin disorder, we must initially observe and understand the properties of the receptor on a cell.
Insulin is, at its very simplest, a growth factor. This means, in short, that it promotes cell longevity and proliferation. Growth factors could lead to a plethora of anti-aging medicines. And just so, we can also realize that an enormous risk factor for Alzheimer’s disease is aging. Certainly, if aging is happening, insulin reception is not (or at least not as well as it normally does). This is the first connection of Alzheimer’s with insulin resistance.
But if that were the only connection, it would likely be coincidence. We must delve deeper into the causes of Alzheimer’s, or at least the causes doctors have identified thus far. The beta-amyloid plaque has been used as the sure-sign of Alzheimer’s for decades. This is an aggregation of protein that essentially clogs up neurons and eventually causes their degeneration. But what could these beta-amyloids have to do with insulin resistance? The answer lies in competition.
Many body receptors have a certain ligand/molecule they like to bind to, but nothing is perfect, and other molecules can also bind instead. It has been proposed that beta-amyloid plaques can bind to insulin receptors on neurons and essentially cause them to not recognize when insulin is actually present. This leads to the opposite effect of the insulin “growth factor” and instead causes the cell to degenerate. Even further, since the cell is recognizing that many of these receptors are full of binding molecules, it “decouples” the receptors from the membrane, making insulin signaling even more difficult.
In reverse, studies have indicated that low levels of insulin reception cause levels of beta-amyloid plaques to increase, exacerbating the problem. There is still no consensus on whether low insulin reception initially creates high levels of beta-amyloid, and this feedback causes lower levels of insulin reception, or whether high levels of beta-amyloid begin the process. Either way, this emphasizes the “insulin resistance” that is so common with diabetes.
All of this culminates in the treatment for Alzheimer’s. A newly-prescribed medicine is intranasal insulin spray. By introducing the molecule to the nasal membranes, it quickly makes its way into the brain, increasing insulin levels. These increased levels might be able to “push” the beta-amyloid plaques out of the insulin receptors and allow normal binding and signaling to occur. Whether this is actually the case is unknown, but the medicine shows promising results.
Is this just one more reason to eat a healthy diet and exercise frequently? Perhaps. But in the end, the choice is our own. We must simply realize that our actions today have an effect on us for the rest of our lives.
Type III Diabetes: Alzheimer’s Disease
