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Amyotrophic lateral sclerosis (ALS) has familial and sporadic forms that follow a similar clinical course. Mutations in the Cu/Zn superoxide dismutase gene (SOD1) have been shown to be a cause of 10 to 20% of cases of familial ALS. In the more common sporadic ALS, SOD1 is not a risk factor. So what else could be mutated in familial ALS or a risk factor for sporadic ALS? One approach is to examine a candidate gene for mutation in familial cases or to look for an increased frequency of a particular nucleotide change (single nucleotide polymorphism [SNP]) in sporadic ALS. Using this approach in this issue of Neurology®, Niemann et al.1 have chosen to examine the GRIN3B gene, which encodes a motor neuron-specific inhibitory subunit of the NMDA receptor (NR3B). They report no mutation of GRIN3B in familial ALS and no association of any SNPs with sporadic ALS. Interestingly they report a 4-bp insertion that truncates the NR3B protein and makes it nonfunctional. This null allele was found in both controls and patients with ALS with equal frequency which provides compelling evidence that NR3B in humans does not give an …
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