Lysosome Dysfunction May Be Key to Alzheimers Disease Pathology

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An abnormal build-up of proteins such as amyloid beta in the brain is often the focus of research into finding the source and ultimately a cure for Alzheimer’s and other neurodegenerative diseases. However, amyloid, though important, is just one of the many toxic proteins that cause brain cell dysfunction, says Ralph A. Nixon, professor of psychiatry and cell biology at New York University's Langone Medical Center and the Nathan Kline Institute. His research focuses on the dysfunction of lysosomes which serve to rid the cells of waste products.

In the cells, disposing of “garbage” or cell waste such as damaged proteins is accomplished by the lysosome, organelles that are present in nearly every cell. Lysosomes hold a variety of enzymes that digest or breakdown complex molecules and pieces of cell. If there is a dysfunction in this process, an accumulation of cellular waste builds-up and contributes to health problems, particularly the degeneration of nerve cells.

Read: Low Level of Key Proteins May Play Role In Alzheimer's Memory Loss

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Dr. Nixon has tested his theory in animal experiments. He was able to prevent cognitive decline in animal experiments by improving the functioning of the enzymes in the lysosomes so that waste products were degraded and processed faster.

"The sheer bulk of waste proteins that are accumulating within the neurons in Alzheimer's disease brains is enormous,'' Nixon says. Ideally, drugs could be developed to repair the defective mechanism early in the disease process before damage is done to the brain.

Read: Senate Passes National Alzheimer's Project Act

Other genetic conditions have been linked to a buildup of cellular toxins as well, including Tay-Sachs disease and Gaucher disease. Nixon and fellow researcher Haoxing Xu of the University of Michigan, who has also been working on lysosome research, says that a better understanding of the lysosome functions could possibly also lead to treatments for Huntington’s disease, Neimann-Pick Type C (NPC), amyotropic lateral sclerosis and Charcot-Marie-Tooth (CMT) disease.

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