Hardiman’s work is focused on what causes ALS. She and colleagues identified angiogenin as a gene mutated in both sporadic and familial ALS (see ARF related news story and Greenway et al., 2006). Angiogenin promotes blood vessel growth and also participates in neurite extension (Subramanian et al., 2008). In another paper, Hardiman and others performed a genomewide association screen to pick out DP66, which encodes a protein that helps make up potassium channels, as a gene associated with risk for developing ALS (see ARF related news story and Cronin et al., 2008).

In contrast, Cudkowicz focuses not on the source of ALS but on how to treat it. She has led clinical trials of potential ALS therapeutics, such as recent evaluations confirming the safety of the drugs sodium phenylbutyrate (Cudkowicz et al., 2008) and arimoclomol (Cudkowicz et al., 2008). Currently, there is only one FDA-approved treatment for ALS, riluzole, and more effective drugs are urgently needed. However, scientists have struggled to find drugs that work as well in people as they do in mice (see ARF Live Discussion).

Hardiman and Cudkowicz will each receive $25,000 to be put toward further ALS research during the AAN’s 61st Annual Meeting in Seattle, to be held April 25 through May 2, 2009.—Amber Dance.