[ed note: Michael Jorrin, who I like call “Doc Gumshoe,” is a longtime medical writer who shares his thoughts with us a couple times a month — his articles are non-financial in nature, his words and opinions are his own, and you can see his bio and his past pieces here. Enjoy!]
Indulge me while I spin an anecdote that might have a tiny bit of relevance to Alzheimer’s disease.
In the dawn of the automobile age – and, no, I am not old enough to remember it! – the circuit that triggered the self-starter was called the “make-and-break.” In Cuba, where I was born and lived as a small child, this became the mequembreque. And when the car would not start, this was attributed to borronilla en el mequembreque. “Borronilla” literally means “eraser crumbs,” but the word is used loosely to describe crud in general. Then, when my father felt a mite under the weather, he would sometimes attribute it to borronilla en el mequembreque _i.e. nonspecific crud in the system.
When I think about AD, and in particular to the various root causes that are being investigated – amyloid beta (Aβ), tau protein, inflammation, toxins, fungi, life-style factors – I am irresistibly drawn to borronilla en el mequembreque. Any or all of those factors produce crud in the system, and this crud interferes with brain function. I do not say that continuing research into the pathophysiology of AD is in vain, and that scientists should just throw up their hands and accept the generalized crud hypothesis. No indeed! That research needs to continue. But the real test is whether reducing the buildup of crud results in getting the car going.
We have seen evidence that some individuals with abundant quantities of brain crud – e.g., amyloid plaque – do not experience significant cognitive decline. We cannot say whether this is because amyloid plaque is not really the root cause of AD or because these individuals have redundant cognitive resources. I suspect the latter. Yes, the buildup of Aβ in the space between neurons blocks some synapses, but these persons have other neuronal links that haven’t been clogged by crud, and their brains continue to function.
It is in the nature of scientists to search for single causes. The direct line from cause to effect is the prized goal of much research, and success is marked by the discovery of the means of interrupting that direct line: block the cause and the effect does not occur. This is the ultimate goal of a lot of AD research. If the buildup of Aβ plaque is the unitary cause of AD, and a means of preventing this buildup is found, and preventing that buildup then prevents the development of the characteristic AD symptoms, then the battle is won.
But so far, as we know, the battle has not been won – far from it! And not just relative to Aβ buildup, but relative to all the proposed causes of AD. In fact, up to now, evidence has been scanty that strategies that address any of the putative causes of AD result in significant clinical benefits.
That’s not a reason to quit trying. AD researchers are no doubt aware of the huge gap between the identification of cholesterol as the substance that forms arterial plaque and the first reliable data that lowering cholesterol improved survival in persons at risk for heart disease. Before 1910 there was extensive demonstration not only of the presence of cholesterol in arterial plaque, but that animals fed a diet rich in cholesterol developed atherosclerosi