Alzheimer’s Drug Research – A Ray of Hope

Read Finding Suggests New Target for Alzheimer’s Drugs, by New York Times science reporter Gina Kolata, to learn about a new direction in Alzheimer’s disease research. In her article Kolata writes about Nobel Prize winner (2000) Paul Greengard, an 84-year-old scientist, who is studying a specific protein, gamma secretase activating protein, that can possibly be targeted by drugs to stop the production of beta amyloid, which is responsible for the progression of Alzheimer’s disease. Dr. Greengard is the Vincent Astor Professor and director of the Fisher Center for Alzheimer’s Research, at Rockefeller University in New York City. An article about his research (abstract) is published in Nature. Moreover, a quick search on PubMed reveals that Professor Greengard’s name has appeared on 16 scientific papers published this year.

Click to see large version at the Times.

According to a Rockefeller University press release:

In Alzheimer’s disease, the problem is amyloid-β, a protein that accumulates in the brain and causes nerve cells to weaken and die. Drugs designed to eliminate plaques made of amyloid-β have a fatal problem: they need to enter the brain and remove the plaques without attacking healthy brain cells. A new breakthrough …  suggests that treatments modeled on the blockbuster cancer drug Gleevec could be the solution.

Dr. Greengard’s research news is interesting for aging parents, but it may provide a much-needed glimmer of hope to adult children, who are now entering the period of life when Alzheimer’s disease begins to occurs more frequently.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s