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Amyloid Plaques & Alzheimer's

Dec 15, 2010 | By Robert DiPardo
Amyloid Plaques & Alzheimer's
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Alzheimer's disease is a neurodegenerative brain disease that relentlessly diminishes memory and mental capacity. Some scientists believe one cause of the death of brain nerve cells in Alzheimer's patients is the formation of amyloid plaques in the spaces between the cells. These sticky plaques consist of fragment proteins formed by the abnormal processing of amyloid precursor protein.

The Facts

Amyloids are small proteins produced when larger proteins are cleaved by normal body processes. Amyloid precursor protein occurs in the brain in the area where a nerve signal crosses from one nerve cell to another. In a normal brain, amyloid precursor protein is cut into specific pieces, amyloids, and these pieces are further broken down and eliminated from the body. In a brain afflicted with Alzheimer's disease, excessive numbers of amyloids are generated, and they clump together to form plaques. The plaques are water insoluble and take up residence in the spaces between the nerve cells in the brain. Scientists believe as these plaques grow larger, they begin to disrupt communication among nerve cells and eventually damage and destroy the cells. As more and more nerve cells die, the clinical signs of Alzheimer's disease, such as memory loss and problems with daily tasks, become evident.

Expert Insight

An article in the February 6, 2008, issue of "Scientific American" discusses research performed by Dr. Bradley Hyman at the Massachusetts General Institute for Neurodegenerative Diseases on the formation of amyloid plaques in a mouse model of Alzheimer's disease. Using a laser microscopy technique, Hyman and his colleagues observed plaque formation in the mouse brain before they saw any evidence of nerve cell degeneration. Results of this research support the theory that amyloid plaques are the cause of Alzheimer's disease.

Potential

In the February 2010 issue of "The FASEB Journal," Mayo Clinic researchers in Jacksonville, Florida, describe the use of a mouse model of Alzheimer's disease to assess the effects of mouse interleukin-6 on the formation of amyloid plaques. Interleukin-6 is a protein that facilitates communication among cells and promotes an inflammatory response. The researchers found that interleukin-6 diminished the deposition of amyloid plaques in the mouse brain, and caused mouse brain immune cells to engulf and digest amyloid plaques in cell culture experiments. They suggest interleukin-6 could be a potential treatment for Alzheimer's disease because the immune response it induces may clear amyloid plaques from the brain.

New Knowledge

An article in "Harvard Gazette" describes how Dr. Brian Bacskai and his team at the Massachusetts General Institute for Neurodegenerative Disease sought to answer two long-standing questions about Alzheimer's disease: do amyloid plaques damage nerve cells in the brain and if so, how? Their research, published in the July 31, 2008, issue of the journal "Neuron," shows that calcium levels in the nerve cells of the mouse brain are much higher if amyloid plaques are present relative to the levels in a brain without plaques. They further determined that these elevated calcium levels interfere with the transmission of nerve signals and cause damage to the nerve cells.

The Future

Alzheimer's disease is now a top priority of scientists working in the field of biomedical research. Understanding of the role of amyloid plaques in the course of the disease has evolved greatly over the last 15 years, and effective and novel treatments that stem from this understanding are within the realm of possibility.

References

Article reviewed by joyce sexton Last updated on: Dec 15, 2010

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