|
|
|
David
Borchelt |
 |
| Dr.
Borchelt’s laboratory is dedicated to gaining a better understanding
of the molecular mechanisms underlying Alzheimer’s disease and
related disorders. |
 |
Professor of Neuroscience
Director, Santa
Fe Health Alzheimer’s Disease Research Center; Investigator,
McKnight Brain Institute
Training
PhD, Microbiology/Virology, Univ. of Kentucky, 1986
MS, Microbiology, Univ. of Kentucky, 1984
BS, Biology, Univ. of Kentucky, 1979
|
Contact
phone:
352.294.0105
office: MBI L1-100D
lab: MBI L4-166
email:borchelt@mbi.ufl.edu
|
|
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.
|
| Research
Associates |
|
| Guilian
Xu , Ph.D. |
Assistant Research Scientist |
| |
|
|
Recent
Publications
Characterization of huntingtin pathologic fragments in human HD, transgenic mice, and cell models. Schilling G, Klevytska A, Tebbenkamp A, Juenemann K, Cooper J, Gonzales V, Slunt H, Poirer M, Ross CA, Borchelt DR J. Neuropath. Exp. Neurol. 2007 66:313-320.
Disease-associated mutations at copper-ligand histidine residues of SOD1 diminish the binding of copper and compromise dimer stability. Wang J, Caruano-Yzermans A, Rodriguez A, Scheurmann J, Slunt HH, Cao X, Gitlin J, Hart PJ, Borchelt DR. J. Biol. Chem. 2007 282:345-352.
Mapping superoxide dismutase 1 domains of non-native interaction: roles of intra and intermolecular disulfide bonding in aggregation.Wang J, Xu G, Borchelt DR. J Neurochem. 2006 96:1277-1288.
Persistent amyloidosis following suppression of Ab production in a transgenic model of Alzheimer’s disease. Jankowsky J, Slunt HH, Gonzales V, Savonenko AV, Wen J, Jenkins NA, Copeland NG, Younkin LH, Lester HA, Younkin SG, Borchelt DR. PLoS Med. 2005 2:e355.
|
|
|
