Belmont Village Quarterly Newsletter
on Senior Living

Alzheimer's Update: Scientists Begin to Untangle Root Cause

November is National Alzheimer’s Awareness Month, and we are pleased to share some of the latest research findings that could, in time, pave the way for the development of new therapeutic drugs.

An estimated 35.6 million people worldwide will be living with Alzheimer’s disease (AD) in 2010 and nearly five million Americans are currently believed to have the disease. As our populations age, these numbers are expected to nearly double every 20 years, according to the 2009 World Alzheimer’s Report, released from Alzheimer’s Disease International (ADI) on September 21. 

Research conducted by the University of California – Los Angeles (UCLA) and published online in the Proceedings of the National Academy of Sciences (PNAS) indicates that we may need to change the way that we think about the cause of AD. 

Scientists have long suspected that a small amyloid beta protein is the cause of AD.  The protein clumps or binds to itself and eventually changes chemically to create the characteristic brain protein deposits (plaques) that have in the past been viewed as a potential cause of AD. However, recent studies have suggested that the cause may be the grape-like clusters of amyloid beta protein themselves, rather than the resulting plaques.

The clusters vary in size, and the relationship between cluster size and their ability to kill nerve cells (toxicity) has been the subject of recent research. UCLA neurologists have determined that toxicity increases dramatically as clusters increase in size. Additionally, the researchers report that although the larger clusters are more toxic than smaller ones, they are relatively rare. The smaller versions are numerous and collectively more toxic.

"We now have the best understanding yet of what types of toxic A-beta structures we should target with new classes of therapeutic drugs," says David Teplow, Ph.D., senior author and a professor of neurology at UCLA.  Teplow further asserts that developing the ability to create these clusters in a way that precisely duplicates what forms in the AD brain will allow scientists to better study their structures, which could also make the development of future therapeutic drugs easier and possibly more successful. 

In other findings published online in The FASEB Journal, researchers reported that the N60 section of a protein called "RanBP9" might be the key that unlocks an entirely new class of Alzheimer's drugs, and with them, hope. "Alzheimer's might seem hopeless to some, but this research shows that we're closer than ever to unraveling both the protein tangles and mysteries surrounding this devastating disease," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal.

Included in their research findings, scientists demonstrated the N60 fragment of the RanBP9 protein increases the production of the amyloid beta protein, which is present in excessive amounts in the brains of people with AD. Most experts believe that if the creation of amyloid beta protein can be halted or slowed, the devastating effects of AD may also be slowed or stopped. Knowing which portion of RanBP9 to target is particularly important because it gives researchers a more specific focus for developing new Alzheimer's drugs.

According to the U.S. Centers for Disease Control and Prevention, Alzheimer's disease is the most common form of dementia among older adults. Alzheimer's disease involves parts of the brain that control thought, memory, and language and can seriously affect a person's ability to carry out daily activities. The disease usually begins after age 60, and risk goes up with age. About five percent of men and women ages 65 to 74 have Alzheimer's disease, and nearly half of those aged 85 and older may have the disease. 

Sources for this article include:
www.alz.org
www.scienceblog.com
www.fasebj.org

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