Wednesday, October 6, 2010

Boston Globe Bestsellers: Sept. 26-Oct. 3

Hardcover Nonfiction (LOOK WHO'S AT #5)

1. Earth (The Book)
By Jon Stewart. Grand Central.

2. The Grand Design
By Stephen Hawking and Leonard Mlodinow. Bantam.

3. The Warmth of Other Suns
By Isabel Wilkerson. Random House.

4. Sh*t My Dad Says
By Justin Halpern. It.

5. The Thousand Mile Stare
By Gary Reiswig. Nicholas Brealey.

6. A Journey (tie)
By Tony Blair. Knopf.

6. Let’s Take the Long Way Home
By Gail Caldwell. Random House.

6. The Power
By Rhonda Byrne. Atria.

6. The Big Short
By Michael Lewis. W. W. Norton.

10. Outliers
By Malcolm Gladwell. Little, Brown.

Saturday, October 2, 2010

REPORT FROM THE RESEARCH FRONT

Since the discovery in 1984 that the plaques found in the brains of people with Alzheimer’s was made up of Beta Amyloid Protein, it has been assumed by many that Beta Amyloid was a major cause of the disease. More than 7,000 research papers have been written, most assuming Beta Amyloid plays a major role in the development of Alzheimer’s. Recently, this has been demonstrated to be true, but not in the way many researchers expected.
Within the past few months, Alzheimer’s research has been rocked with news about the ineffectiveness of experimental treatments that prevent the formation of, or reduce the amount of, plaque in the brains of people living with Alzheimer’s. Because of these failures, the Manhattan chapter of the Alzheimer’s Association brought together five prominent researchers who discussed, PARADIGM SHIFTS IN ALZHEIMER’S RESEARCH: IMPLICATIONS FOR DIAGNOSIS AND TREATMENT. Here’s some of what I learned at the two-hour presentation.
Instead of causing the disease, plaques in the brain apparently result from an immune response, an attempt to fight off disease. This explains why the treatments in research models that lowered the amount of visible plaque actually made patients worse. It could also explain why some people who show a large amount of plaque in their brains do not have symptoms of dementia.
Several research projects will now focus on oligomers, a more soluble form of the protein, while other researchers will concentrate on tau, the other prominent protein comprising the neurofibulary tangles, the second, long recognized abnormal accumulation found in the brains of people with Alzheimer’s. The search is now on for a compound that will attach to and identify oligomers, similar to the radio-active compounds that currently can be used to find Beta Amyloid in the brain.
The more than sixty private companies involved in Alzheimer’s research have spent billions of dollars trying to find an effective treatment, but, so far, major advances have eluded everyone. However, the point is well taken that each setback is an advance in knowledge. The positive news is twofold: Beta Amyloid does not appear to be the culprit it was once thought to be, and is not likely the key to prevention of the disease, so attention can now be focused elsewhere; and, the private companies, in addition to publicly funded laboratories, are all still involved in trying to find answers despite the fact their investments so far have brought no financial rewards.
One researcher quipped, “We’ve cured a lot of animals (rats and mice) that we’ve purposefully infected with Alzheimer’s. We’re making progress.” Another observed, “Apparently, it is easier to send a man to the moon than to find an effective treatment for Alzheimer’s. That’s how complex the disease is.”
Mary Sano, PhD, director of the Alzheimer’s Disease Research Center at the Mount Sinai Hospital School of Medicine, observed that more volunteers are needed to participate in research. She reminded everyone that the Alzheimer’s Association has a program to match volunteers with appropriate ongoing research. www.alz.org.