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Over the past few years scientists have identified genes that are suspected in the development of Alzheimer’s disease. They are just beginning to piece together what Alzheimer’s related proteins do in the cell, and how they contribute to the development of the disease.

Lawrence Godstein, Howard Hughes Medical Institute, and colleagues at the University of California, San Diego, studied amyloid precursor protein (APP), which develop into abnormal amyloid clumps—amyloid-beta is suspected to contribute to the death of nerve cells that leads to the development of Alzheimer’s disease.

Using mouse neurons as a model, the scientists showed that APP is an attachment point for a molecular motor called kinesin. Kinesin transports packets of protein from the main cell body along the length of the cell, which is crucial to nerve cells. These nerve cells have the unique property of sending out tendrils, called axons, up to several feet from the main cell body to distant parts of the body.

When something goes wrong with the transport process of the tendrils, the cell often cannot cope and sends out a distress signal that initiates the death of the cell. The researchers have concluded that APP may be involved in the signaling process that leads to the cell’s death when nerve cells are damaged.

Researchers also discovered that 2 other key proteins linked to Alzheimer’s disease, beta-secretase and presenilin-1, are found with APP. Beta-secretase and presenilin-1 are thought to be the main enzymes that process APP and create amyloid-beta. Finding them together inside the cell suggests that APP may be part of a normal cell transport function that is somehow disrupted in Alzheimer’s disease.

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