Mitchell J, Paul P, Chen HJ, Morris A, Payling M, Falchi M, Habgood J, Panoutsou S, Winkler S, Tisato V, Hajitou A, Smith B, Vance C, Shaw C, Mazarakis ND, de Belleroche J. Familial amyotrophic lateral sclerosis is associated with a mutation in D-amino acid oxidase. Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7556-61. PubMed.
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University of Arkansas for Medical Sciences
Regarding the statement in this news story "De Belleroche also pointed out that a DAO mutant mouse might be a useful model for ALS research, which sorely needs new models," I'd like to note that it is unlikely that loss of DAO alone will be sufficient for disease. A line of DAO mutant mice, essentially devoid of DAO activity, has been around almost 30 years (Konno and Yakumura, 1983) without any ALS-like symptoms reported in the first year of life. Here is a quote from that paper:
"No apparent difference was detected between DAO+ and DAO- mice. The DAO- mice grew and behaved normally. They were fertile and produced as many offspring as the DAO+ animals did. Besides, the unilaterally nephrectomized DAO- mice lived more than 1 year without any impairment of health. ... [T]he discovery of the DAO- mice suggests that the enzyme is not essential, at least for the growth and reproduction of the mouse under laboratory conditions."
References:
Konno R, Yasumura Y. Mouse mutant deficient in D-amino acid oxidase activity. Genetics. 1983 Feb;103(2):277-85. PubMed.
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