In this issue of Neuron, Suh etal. (2013) describe two rare ADAM10 prodomain mutations that cause late-onset Alzheimer@s disease by impairing prodomain chaperone function, attenuating α-secretase activity, and reducing adult hippocampal neurogenesis. These results support both ADAM10 as a therapeutic target and the amyloid hypothesis of Alzheimer@s disease.
|Original language||English (US)|
|Number of pages||4|
|State||Published - Oct 16 2013|
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