ADAM10 prodomain mutations cause late-onset alzheimer's disease: Not just the latest FAD

Robert Vassar

doi:10.1016/j.neuron.2013.09.031

ADAM10 prodomain mutations cause late-onset alzheimer's disease: Not just the latest FAD

Robert Vassar^*

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Short survey › peer-review

24 Scopus citations

Abstract

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)
Pages (from-to)	250-253
Number of pages	4
Journal	Neuron
Volume	80
Issue number	2
DOIs	https://doi.org/10.1016/j.neuron.2013.09.031
State	Published - Oct 16 2013

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuron.2013.09.031

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title = "ADAM10 prodomain mutations cause late-onset alzheimer's disease: Not just the latest FAD",

abstract = "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.",

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AB - 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.

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ADAM10 prodomain mutations cause late-onset alzheimer's disease: Not just the latest FAD

Abstract

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