Defective cell transport suggested in Alzheimer...( nt one of the first detailed studies of...)

Defective cell transport suggested in Alzheimer's disease

nt one of the first detailed studies of amyloid-beta being formed in compartments inside living nerve cells.

To complement the mouse studies, the researchers studied the effects of various APP gene mutations in fruit flies. As reported in the Neuron article, Goldsteins team showed that excess APP containing amyloid-beta region and the C-terminus caused neural cell death, but amyloid-beta containing APP alone did not. These results and research by other investigators led Goldstein's team to conclude that the C-terminus may carry a cell death signal that can be initiated when transport fails.

Our results suggest maybe it is the cleavage to liberate this C-terminal piece that is sending a signal back to the cell body to die, said Goldstein. It certainly is an interesting clue and makes sense in the context that if a cell is damaged it needs to be able to signal to the nucleus.

The results also are consistent with the epidemiological observation that people who suffer trauma to the brain are more susceptible to developing Alzheimers disease, Goldstein added. The investigators are now trying to isolate the death signal for further study.

While Goldstein says the results are not definitive, he suggests studies such as these should help sort out the question of which protein products lead down the path to cell death seen in Alzheimers disease.

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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
5-Dec-2001

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