Dr. David Borchelt

Dedicated to gaining a better understanding of the molecular mechanisms underlying Alzheimer’s disease and related disorders.

Dr. David BorcheltProfessor of Neuroscience
Director, SantaFe Health Alzheimer’s Disease Research Center;
Investigator, McKnight Brain Institute & CTRND
PhD, Microbiology/Virology, Univ. of Kentucky, 1986
MS, Microbiology, Univ. of Kentucky, 1984
BS, Biology, Univ. of Kentucky, 1979




Contact Dr. Borchelt
Phone: 352-273-9664
email: borchelt@mbi.ufl.edu

Research Focus and Aims
Over the past several years there has been tremendous progress in identifying the gene products that mediate a number of neurodegenerative disorders, including familial Alzheimer’s disease, familial amyotrophic lateral sclerosis, and Huntington’s disease. These disorders are all progressive, fatal disorders that result from the dysfunction and death of specific populations of nerve cells. In all of these disorders, a change in the amino acid sequence of specific proteins initiates a cascade of events that lead to disease. A common feature of these disorders is the accumulation of misfolded proteins or peptides in regions of the CNS affected by each disease. My laboratory is committed to investigations designed to elucidate the molecular processes by which specific mutant proteins cause disease. This work involves the use of transgenic mouse models, knockout mice, and cell culture systems to examine the effect of mutations on the function and biology of the mutated proteins. Collectively, these approaches provide insight into the molecular mechanisms of disease and have the potential to identify new therapeutic strategies for these disorders.
Recent Publications

  • Melnikova T, Fromholt S, Kim H-S, Lee D, Xu G, Price A, Moore BD, Felsenstein KM, Savonenko A, Borchelt DR. Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis. J Neurosci, 33:3765-79, 2013. PMID:23447589. PMCID: PMC3711622.
  •  Xu G, Stevens Jr SM, Moore BD, McClung S, Borchelt DR. Cytosolic proteins lose solubility as amyloid deposits in a transgenic mouse model of Alzheimer-type amyloidosis. Hum Mol Genet, 22:2765-2774., 2013. PMID:23512986.
  •  Price AR, Xu G, Siemienski ZB, Smithson LA, Borchelt DR, Golde TE, Felsenstein KM. Comment on “Apoe-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models”. Science, 340:924., 2013. PMID23704553.  
  •  Chan P, Chattopadhyay M, Sharma S, Souda P, Gralla E, Borchelt DR, Whitelegge JP, Valentine JS. Structural analysis of superoxide dismutase-1 fibrils using limited proteolysis and atomic force microscopy. Proc Natl Acad Sci USA, 110:10934-10939., 2013. PMID:23825679; PMCID: PMC3704032.
  •  Chakrabarty P, Rosario A, Cruz P, Siemienski Z, Ceballos-Diaz C, Crosby K, Jansen K, Borchelt DR, Kim JY, Jankowsky JL, Golde TE, Levites Y. Capsid serotype and timing of injection determines AAV transduction in the neonatal mice brain. PLoS One, 8:e67680., 2013 PMID:23825679. PMCID:PMC3692458.
  •  Ayers J, Lelie H, Workman A, Prudencio M, Brown H, Fromholt S, Valentine J, Whitelegge J, Borchelt D. Distinctive features of the D101N and D101G variants of superoxide dismutase 1; two mutants that produce rapidly progressing motor neuron disease. J. Neurochem. Epub, 2013. PMID:24032979.

PubMed hyperlink