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Last updated on April 17, 2014 at 1:21 EDT

Second Part of Alzheimer’s Toxic Two Identified

February 10, 2011

(Ivanhoe Newswire) — Like two brothers wrestling fighting who need to be put in separate corners, a pair of protein molecules work together to speed up the toxic events of Alzheimer’s disease. The second molecule was identified and could lead to novel drugs that slow or even prevent the disease.

Alzheimer’s disease is an irreversible, progressive brain disease marked by deterioration of nerve cells and eventual complete loss of cognitive functioning ““ thinking, memory, and reason. Many Alzheimer’s patients have brain lesions called amyloid plaques, which consist of protein fragments called amyloid-beta. Small aggregates of amyloid-beta are thought to contribute prominently to the degeneration of brain cells in Alzheimer’s.

The discovery involves an amyloid beta fragment called AICD. Scientists have known that AICD controls expression of genes that contribute to Alzheimer’s, but how it did so was unclear ““ until now. “We discovered a protein molecule that communicates with AICD to turn on target genes,” Thomas G. Boyer, Ph.D., professor of molecular medicine at the Health Science Center, was quoted as saying. “We hope to exploit this knowledge to identify compounds or drugs that can disrupt these signals, leading to a novel and effective treatment for this disease.”

Alzheimer’s disease is the most common cause of dementia among older people, and estimates indicate that as many as 5.3 million Americans suffer from it. While several drugs approved by the U.S. Food and Drug Administration can temporarily slow worsening symptoms, no treatment is currently available to slow or stop the degeneration of nerve cells that lies at the root of the disease.

SOURCE: EMBO, published online February 4, 2011