(Picture of a GSM from CIPS.)
The reason, as the Mayo Clinic notes, lies in how they work, by reducing production of long pieces of the amyloid beta protein (Abeta) that form clumps, while increasing production of shorter strings of the same protein that can keep the longer strings from sticking together.
Think of how rice cooks. Short grain rices stick together in a risotto. Long grain rises remain separate in a pilaf. The reason is the mix of proteins in the different rice grains.
In this case you're talking about different versions of the same protein but it's the same effect. Better your blood is a pilaf than a risotto.
In controlling this process you control the creation of plaque, which clogs the brain arteries of Alzheimers' patients, killing them slowly. But plaque is also the cause of heart attacks, clogging arteries feeding the heart muscle, killing folks quickly.
What makes GSMs so promising is that, while statins may stop plaque from forming they do nothing about plaque which is there, while with the new drugs "GSM agents actually stick to the Abeta already in the brain, keeping it from aggregating."
Senior study author Tony Golde was quite explicit in the link between the diseases:
“In a very general sense the action of these GSM on Abeta might be analogous to some cholesterol lowering drugs that can lower LDL, the bad cholesterol that sticks to your arteries, and can raise HDL, the good cholesterol that sweeps out LDL.”
Five months ago, in the Fight over Statins, I casually mentioned studies of statins and Alzheimers, some of them contradictory, suggesting the problem in both cases is the same as with Atlanta traffic, clogged arteries.
A personal note here. My father died of heart disease, my grandfather of Alzheimer's. The idea of them having similar risk factors and causes is not foreign to me.
All this is a long way from making it to your loved one's bedside. But perhaps we can get it to yours and mine.