Christopher Shaw received the Sheila Essey Award 24 April at the American Academy of Neurology (AAN) meeting in New Orleans, Louisiana. Shaw, of King’s College London, U.K., received the $25,000 prize for his work to discover genetic mutations underlying amyotrophic lateral sclerosis (ALS). The AAN and the ALS Association (ALSA) jointly presented the Essey award. The two organizations debuted another award earlier this year: a three-year fellowship for young clinician-scientists. The new Richard Olney Clinician Scientist Development Award in ALS bears the name of the former director of the ALS Treatment and Research Center at the University of California, San Francisco. Olney died in January of the same disease he had worked to treat for many years.

Shaw co-discovered key ALS genes, including TAR DNA binding protein 43 (TDP-43; see ARF related news story on Sreedharan et al., 2008) and fused in sarcoma (FUS; see ARF related news story on Vance et al., 2009). He has also contributed to studies of other ALS genes including superoxide dismutase 1, and to the banking of DNA from people with ALS and their families. Essey award recipients typically use the money to fund research projects or trainees. The award honors Sheila Essey, who died of ALS in 2004.

Richard Olney passed away January 27 at the age of 64. He had directed the ALS Treatment and Research Center until his illness forced him to retire in 2004. From that point on, he shared his experiences with the public to boost awareness of the disease and funds for his center. He received a Public Education Award from the AAN Foundation in 2006. Olney also continued to participate in research as a trial subject. The Olney Fellowship, announced in February, is accepting applications and will provide $80,000 per year for salary and educational expenses to an early-career neurologist pursuing clinical research on ALS.—Amber Dance.


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News Citations

  1. Gene Mutations Place TDP-43 on Front Burner of ALS Research
  2. New Gene for ALS: RNA Regulation May Be Common Culprit

Paper Citations

  1. . TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis. Science. 2008 Mar 21;319(5870):1668-72. Epub 2008 Feb 28 PubMed.
  2. . Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6. Science. 2009 Feb 27;323(5918):1208-11. PubMed.

External Citations

  1. award
  2. passed away
  3. experiences
  4. Olney Fellowship
  5. applications

Further Reading


  1. . Familial amyotrophic lateral sclerosis with frontotemporal dementia is linked to a locus on chromosome 9p13.2-21.3. Brain. 2006 Apr;129(Pt 4):868-76. PubMed.
  2. . Two families with familial amyotrophic lateral sclerosis are linked to a novel locus on chromosome 16q. Am J Hum Genet. 2003 Aug;73(2):390-6. PubMed.
  3. . No association of the SOD1 locus and disease susceptibility or phenotype in sporadic ALS. Neurology. 2004 Dec 28;63(12):2419-22. PubMed.
  4. . CHMP2B mutations are not a common cause of familial or sporadic amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry. 2008 Jul;79(7):849-50. PubMed.