Huntington
Potter, Ph.D.
Professor
in the Department of Biochemistry and Molecular Biology Eric Pfeiffer
Chair for Research on Alzheimer's Disease
E-mail: hpotter@byrdinstitute.org
Phone: 813-974-5369
Training
Student and Professor at Harvard University
Research
Interests
Recently,
Dr. Potter has discovered that a common feature of cancer (chromosome
mis-segregation leading to aneuploid cells) may also be an important cause
of Alzheimer's disease. Specifically, Dr. Potter has been investigating
the relationship between classical Alzheimer's disease and Down Syndrome,
which invariably leads to Alzheimer's by age 30-40. This research has
led to the suggestion that many cases of Alzheimer's disease are caused
by the abnormal accumulation throughout the body of small numbers of cells
with three copies of chromosome 21 (the chromosome abnormality that leads
to Down Syndrome). Interestingly, one of the genes which, when mutant, causes
the majority of inherited Alzheimer's dissease (presenlin) is regulated
by p53 and may be an important effector of p53 mutations. Both Alzheimer's
disease presenilin mutations and p53 mutations/deletions cause chromosome
mis-segregation. The link between cancer and Alzheimer's disease is also
suggested by the finding that transgenic mice lacking presenilin in some
tissues develop tumors in those tissues. These relationships underscore
the need to understand the mechanism by which presenilin and p53 cause
chromosome mis-segregation. This will be one of the goals of the Potter
lab over the next few years.
Search
for publications by: 
This
search will be conducted at the US National Library of Medicine (NLM) and PubMed.
Selected
Publications
1. Potter H, Weir L and Leder P. (1984) Enhancer-dependent expression
of human k-immunoglobulin genes introduced into mouse pre-ß lymphocytes
by electroporation. PNAS 81:7161-7165.
2. Abraham CR, Selkoe DJ and Potter H. (1988) Immunochemical identification of a serine protease inhibitor, a-1 antichymotrypsin, in the amyloid deposits of Alzheimer's disease brain. Cell 52:487-501.
3. Potter, H. (1991). Review and Hypothesis: Alzheimer disease and Down syndrome-chromosome 21 nondisjunction may underlie both disorders. Am. J. Hum. Genet. 48:1192-1200.
4. Ma J, Yee A, Brewer HB, Das S and Potter H. (1994) The Alzheimer amyloid-associated proteins a1-antichymotrypsin and apolipoprotein E promote the assembly of the Alzheimer ß-protein into filaments. Nature 372:92-9.
5. Li J, Xu M, Zhou H, Ma J and Potter H. (1997) Alzheimer presenilins in the nuclear membrane, interphase kinetochores, and centrosomes suggest a role in chromosome segregation. Cell 90:917-927.
Cancer Biology Ph.D. Program
H. Lee Moffitt Cancer Center, MRC-4 East
12902 Magnolia Drive
Tampa, Florida 33612
Phone: 813-745-6876
E-mail: CancerPHD@moffitt.org
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