By now, most of you know that a major scientific meeting of Alzheimer’s disease experts took place in our nation’s capital this week.
There is a lot of excitement about some of the new information reported at the conference that may lead to better treatments within the next few years.
And in my opinion, the most important development highlighted at the conference are some new tools that may finally provide answers about the stuff that Alois Alzheimer, a German physician, first noticed in 1906 when he stared at the brain tissue of a 55-year-old woman who had died in a mental institution of bizarre symptoms involving confusion, memory loss and emotional outbursts.
The “stuff” he was looking at under the microscope is now known to be a sticky protein called beta amyloid. And for years, scientists have debated just what role this protein plays in the cause and/or progression of Alzheimer’s disease. Now, two major developments may provide some answers.
The first is the “vaccine” that has been prominent in the news in recent days. I put the word “vaccine” in quotes because we usually associate that word with something given to prevent disease from occurring in the first place.
In fact, the word really means anything that will stimulate the immune system into action, either before disease occurs to prevent it — or after disease is in place to treat it. In the case of Alzheimer’s disease scientists have been able to inject a form of beta amyloid into mice to stimulate their immune systems to attack beta amyloid in the brains of mice bred with brain damage similar to Alzheimer’s disease.
It worked — the beta amyloid began to melt away in the mice. And this week, scientists announced that early trials to see if a beta amyloid vaccine would be safe in humans have passed that safety test. That means trials for effectiveness in humans should start next year.
The other developments involve drugs that may act to prevent the formation of beta amyloid in the first place. These drugs involve enzymes that interfere with the production of beta amyloid. One such drug is now in safety trials and may be ready for effectiveness trials soon.
If either or both of these attempts to attack beta amyloid work in humans, we will start to answer the question first posed by Dr. Alzheimer himself — is this sticky stuff the real culprit in Alzheimer’s disease? Most scientists are betting that it is a very important culprit but probably not the only one.
In the meantime, there are some treatment approaches that can help stall the progression of the disease — including a new one announced this week that helps boost the memory system. But the real answers will come only when we finally figure out what beta amyloid and other unusual proteins in the brain are doing to lead to the devastating disease that already afflicts more than 4 million Americans.
Finally, we are on the way to those answers.
ABCNEWS Medical Editor Dr. Timothy Johnson has provided commentary for viewers on ABCNEWS’ Good Morning America since the program’s debut in 1975. He also provides on-air analysis of medical news for World News Tonight, Nightline and 20/20. His column appears here every two weeks.