we've got here is failure
to communicate "
As scientists realized that Alzheimer's was not just inevitable "senility," but rather a brain disease, they found one obvious change in the brain: a decrease in acetylcholine, a neurotransmitter that carries signals across synapses between neurons. Like junction boxes in a phone network, synapses allow neurons to reach out and touch one other. Absent neurotransmitters, synapses are less effective than a phone company on a walkout.
Acetylcholine is so vital that deadly chemicals like nerve gas, organophosphate pesticides, botulism toxin and the arrow poison curare all work by interfering with it. Doctors responded logically to the news about acetylcholine reduction: Why not restore the neurotransmitter by adding chemicals that the body can convert to acetylcholine? It was a beautiful theory, but it was overwhelmed by an ugly fact: Supplements of raw materials like choline and lecithin failed to slow Alzheimer's.
A backwards approach to the same problem works rather better. Instead of trying to make more acetylcholine, three new drugs try to preserve the chemical by interfering with an enzyme that decomposes acetylcholine. The so-called "acetylcholinesterase inhibitors" indeed reduce Alzheimer's symptoms -- to some extent, and with considerable side effects.
Grossberg, who has studied rivastigmine for five years, says that while the drug's effects vary depending on the stage of illness, "There is impressive data that rivastigmine may improve and stabilize memory, cognition, intellect, behavior and activity," in individuals with moderate or severe Alzheimer's disease.
While rivastigmine caused nausea in 47 percent of patients during early studies, Grossberg says side effects are greatly reduced if the dosage is slowly increased. Some patients, he says, have been taking the drug for five years.
you getting it?
"I think the diagnosis is not being made early enough," says Grossberg. "Health care providers are not doing a good enough job."
the ideal solution
Nonetheless, Flicker says it's "probably worthwhile" testing the drugs on "quite a large number of patients" and that something is better than nothing. "They are the only available class of treatment where substantial evidence exists for efficacy" (see "Acetylcholine Inhibitors for Alzheimer's..." in the bibliography).
Indeed, while it's more desirable to treat root causes than symptoms, at this point Grossberg says the "Inhibitors produce symptomatic improvements in different domains, and may moderate the progression, buying people more quality, functional time. It's great, it may keep them independent, at home longer, there's less likelihood of institutionalization."
So are any good diagnostic techniques on the horizon?
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