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Unraveling Batten disease
Date:11/2/2011

fficking is disrupted. As a result, certain proteins accumulate abnormally in the lysosome, the cell's waste-recycling machine, instead of being transported to another destination. At some point the lysosome is filled beyond capacity; it then interferes with molecular signaling and other vital processes in the neuron, eventually killing the cell.

A great deal of research must still be performed before this finding benefits humans, but the clarification of the CLN3 function is precisely what might help develop a new therapy. Replacing the defective CLN3 in all the brain's neurons is a daunting challenge, but replacing its function for example, by activating the relevant kinase by means of a drug should be much more feasible.


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Contact: Yivsam Azgad
news@weizmann.ac.il
972-893-43856
Weizmann Institute of Science
Source:Eurekalert

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