Are we going back to "hardening of the arteries?"

According to Google's analytics, people aren't much interested in my reporting on the AAIC conference.  So I'm wondering if I shouldn't go light on that before it hurts my SEO.  In any event, I heard several things this morning that have changed my understanding of Alzheimer's disease.

Yesterday's meetings made news on NPR, the NY Times, the Wall Street Journal, etc.  It was about how close we are to a blood test for Alzheimer's disease, but we're just not quite there yet.  The lectures on how the various candidate tests work were fascinating, but a bit geeky.  So I'll spare you.

But my question remains: What''s taking so long??

The answer seems to be that a set of criteria was established early on for what would constitute a reliable test, and no one has quite met all the end points.  So it continues as a work in progress.

This morning (while on the treadmill) I heard fascinating talks on the role of the vascular system in Alzheiemer's disease and on younger-onset Alzheimer's disease (YOAD).  Both had news in them for me.

Until about 1990, we associated dementia with "hardening of the arteries," the idea being that cholesterol was clogging arteries, and restricted blood flow caused Alzheimer's disease.  This would have to be separate from vascular dementia, although the distinction was emerging slowly.  So they call this understanding a "global" view of the disease because it tries to look at what is happening in the whole brain.

But in the early 1990s, the focus moved to the cellular level, to the amyloid plaques and microtubule tangles that Alois Alzheimer first noted in 1906.  These are associated with individual cell death.  Since then, it's been all about peptides and proteins -- amyloid and tau.  But some research is bringing the global view back into focus.

In this morning's lecture, the researcher discussed a new (to me) idea that the amyloid plaques interact with the vascular system in a way that damages blood vessels and impedes blood flow.  This starves cells for blood-borne nutrients, contributing to their deaths.  This occurs in an environment where oxidative damage is occurring -- so eat your blueberries!  (He also discussed a role for dietary salt in this process, similar to what we discussed here before.)

The second talk I heard was on YOAD, and it offered new information on the role of genetics.

They defined YOAD as any Alzheimer's disease manifesting symptoms before age 65.  I had always thought of it as a variant of older-onset ("sporadic") Alzheimer's disease, and that it was a slightly different disease driven entirely by a specific set of genes.  Well, maybe not.  (This is not entirely resolved, and there are differing opinions.)

It may be that those specific genes will inevitably cause YOAD, but not all YOAD is caused by those genes.  I may need to go back and tweak the text in my book, because this may conflict with what I wrote.

A couple of things he noted about YOAD were that it advances more rapidly than sporadic Alzheimer's disease, and, not coincidentally, leads to earlier death.  Essentially, YOAD cuts about 18 years from someone's life.  However, people with YOAD are a rich population for study, because they have fewer other health complications to confuse a study, and they are easier to identify in the general population.  Being younger, they tend to be more eager to help with research.