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Defective cell transport suggested in Alzheimer's disease

Over the last few years, scientists have been successful in identifying genes implicated in Alzheimers disease, but they are just beginning to piece together what the Alzheimer's-disease-related proteins do in the cell, and how they may cause disease.

Now, Howard Hughes Medical Institute investigator Lawrence Goldstein and his colleagues at the University of California, San Diego, report in the December 6, 2001, issue of the journal Nature that several of these proteins are involved in trafficking cargo inside nerve cells. In a related report published in the November 8, 2001, issue of the journal Neuron, a team of researchers led by Goldstein showed that disruption of the transport system caused by defects in these proteins can lead to nerve cell death.

If you look at the history of breakthroughs in disease, often the understanding of what proteins normally do gives important clues to what is aberrant in disease, said Goldstein. This has been much less useful so far in understanding neurodegenerative diseases. Neurologists see protein aggregations in diseased brains, but there is a big gulf in understanding whether the generation of protein aggregates causes the disease per se.

In the brains of patients with Alzheimers disease, a peptide called amyloid-beta accumulates in areas of the brain where nerve cells die en masse, leading to progressive dementia. Goldstein and his colleagues studied the role of amyloid precursor protein (APP), which gives rise to the abnormal amyloid clumps.

Using mouse neurons as a model, the scientists showed that APP serves as an attachment point for a molecular motor called kinesin, which transports packets of protein from the main cell body along the length of the cell. This cell transport mechanism is crucial to nerve cells, which have the unique property of sending out tendrils, called axons, up to several feet from the
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
5-Dec-2001


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