Tuesday, November 29, 2005

Alzheimer's, One More Time

It was strange, starting that earlier post on caring for parents with Alzheimer's before Thanksgiving. Not long after I posted the aborted version, I heard a show on NPR on the disease that first scared the hell out of me, then gave me much-needed hope.

There's no good online text that says everything I heard on the radio show, so I'll have to reconstitute it from memory. First, the bad news: Alzheimer's is on the rise. There are two main factors driving this: 1) the aging, monolithic baby-boomer generation and 2) increases in longevity. Since more people are getting older (and a lot older) than ever before, many more people are showing signs of Alzheimer's or other senility/dementia. One expert on the show said that we could soon face the prospect of society being divided into two groups: the people with Alzheimer's, and the people who take care of them.

Second, the good news: scientists at Thomas Jefferson University (right here in Philadelphia, employer of my s.o., the lovely and talented Sylvia) might be on the right track to slow, prevent, and/or cure the disease in 5 to 10 years.

It's not so easy. Basically what they've been able to do is study the 10% of people with Alzheimer's whom they believe contracted the disease genetically. What happens in Alzheimer's -- they think -- is that amyloids, made from proteins that are normally found throughout the body, become folded on themselves ("like a bobby pin," Dr. Gandy said) in such a way as to become extrmely gooey, forming plaques which, in turn, are poisonous to brain cells. Researchers are trying to find ways to help the body break down amyloids, through aggressive drug treatment, vaccination, etc. Gandy's team at Jefferson, using this theory of causation and treatment, has been able to induce effects similar to Alzheimer's in a mouse, and then cure the mouse with the appropriate medication to remove the plaques. And just yesterday a Korean team announced that they'd isolated the protein that causes amyloid plaques in Alzheimer's: ERK1/2. If they're right, this could be a big step towards a cure. Gandy says that we might be able to get to the point where we treat Alzheimer's the way we treat high cholesterol.

So what's the problem? Well, there are several. First of all, Alzheimer's might not be caused by amyloids at all, but by some other cause. That's a biggie.

Also, researchers are assuming that genetic and nongenetic Alzheimer's are similar in their mechanical if not ultimate causes and effects. It's possible that genetic and nongenetic Alzheimer's might have slightly different proximal causes (say, a different kind of protein) or respond differently to the same kind of treatment.

Another issue is that because Alzheimer's progresses so slowly, any clinical trials of a new medication would need to run for around a year or so to see if they're having a significant effect in retarding the disease's progress. It's these lengthy trial runs that primarily account for the 5-10 year projection offered by the Jefferson team.

Finally, people aren't mice. The effect of Alzheimer's can be delicate, subtle, and subjective. It's especially unclear how and whether treatment might help the short- and long-term recovery of cognitive abilities, memories, etc. In the worst-case scenario, Alzheimer's medication might be able to clear away the plaques, but the poisoning of the brain cells, once begun, continues unabated.

All in all, it's signs for cautious optimism. I only hope that progress doesn't come too late -- for millions of people, it already has, and for millions more, it certainly will.

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