We learned this week that, at 90 years of age, William Shatner will be flying into space aboard a SpaceX rocket. Good for him. As for me ... I thought about it. No thanks.
There's also some other interesting news about outer space in the realm of Alzheimer's research. We kind of understand how beta amyloid forms in the brain, but not completely. And perhaps a better understanding of this process can help us find a way to stop beta amyloid from forming and damaging, even killing brain cells.
Dr. Amir Hirsha of Rensselaer Polytechnic Institute has come up with the novel idea of studying formation of the renegade peptides we find in Alzheimer's and Parkinson's diseases in a weightless environment -- or rather in "microgravity." Since early August, they have been conducting experiments with insulin on the International Space Station (ISS) to study the formation of amyloid fibrils under special conditions. Initial studies have been with insulin to model the process, and later studies will actually use alpha-synuclein (Parkinson’s) and beta-amyloid (Alzheimer’s) peptides.
Peptides are strings of amino acids that are not long enough to qualify as proteins. Before becoming a peptide, beta amyloid was a protein known as the "amyloid precursor protein," but it was cut into pieces by a couple of enzymes. You will, of course, already know this if you read Beating the Dementia Monster.
The problem with doing the research under normal gravity is that you must conduct it in a container, maybe a test tube, and the containers don't simulate conditions of the brain very well. A part of the process of amyloid fibril formation involves movement of fluids. The forces that exist between layers in moving fluids influence the reactions, and friction with container walls will interfere with the fluid motion.
So what Dr. Hirsha and his grad students are doing is analyzing reactions inside drops of fluid suspended weightlessly inside the ISS. They are able to generate circulation within the drops, clockwise on one end and counterclockwise on the other. This produces the forces between the layers of fluid that more closely resemble what happens inside the brain when the fibrils are formed.
(Fluid mechanics was my worst class in college...)
Where will this lead? I have no idea. But it illustrates both how little we know about how Alzheimer's disease progresses and the ingenuity we are applying to learn what we need to know.
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