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David Pearce, Ph.D.




  • Vice President of Research, Sanford Health
  • Director, Sanford Children's Health Research Center
  • Professor of Pediatrics, USDSSM


  • Postdoctoral Fellow, Biochemistry & Biophysics, University of Rochester, N.Y.
  • Postdoctoral Research Assistant, University of Oxford, U.K.
  • Ph.D., University of Bath, U.K.
  • B.Sc., Biological Sciences, University of Wolverhampton, U.K.

Current Research:

Neuronal Ceroid Lipofuscinoses is caused by autosomal recessive inheritance of mutations in the genes CLN1-10. Juvenile Neuronal Ceroid Lipofuscinosis (Batten Disease) is the most common neurodegenerative disease of childhood resulting from mutations in CLN3. This devastating disease results in loss of vision around age five, followed by slow decline in cognitive and motor function, and a progressively increased frequency of seizures. Batten disease is universally fatal. The Pearce lab uses multiple approaches to investigate the underlying pathological mechanisms of Batten disease.

The following ongoing projects offer graduate opportunities in the Pearce lab:

  • Cell Biology/Biochemistry: (1) We have identified several proteins that physically interact with CLN3. (2) Project 1-Characterization of CLN3 protein-protein interactions and how they regulate CLN3 function. (3) Project 2-Characterization of protein-protein interactions for proteins associated to other forms of Batten disease, namely the CLN6 and CLN8 proteins.
  • Molecular Genetics/Molecular Biology: (1) CLN3 has a homolog in yeast, designated Btn1p. Manipulating this model system is a powerful way to determine the function of a protein. (2) Project 1- Through molecular genetic techniques we are characterizing the function of Btn1p in yeast. (3) Stop mutations in CLN1, CLN2 or CLN3 result in the corresponding mRNA being degraded. (4) Project 2-Investigation and stabilization of mRNAs that bear nonsense mutations as a therapeutic approach to Batten disease.
  • Neuroscience: (1) Project 1-Pathological and behavioral characterization of cln3-mouse models of Batten disease. (2) Project 2-Charcterization of the underlying neurochemical abnormalities in cln1, 2 and 3 mouse models of Batten disease. Targets for therapeutic intervention.
  • Proteomics: (1) Project 1-Characterization of the changes associated to Batten disease in the central nervous system of mouse models for Batten disease.