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Thomas
N. Ferraro, Ph.D.
Research Associate Professor, Dept of Psychiatry
Center for Neurobiology & Behavior
Office - Room 2209; Lab - 2109
Translational Research Laboratory Building
125 So. 31st Street
(215) 573-4581
email: tnf@mail.med.upenn.edu
Click here for selected publications since Dr. Ferraro's arrival at Penn
RESEARCH INTERESTS
Genetic influences in complex traits and behaviors that are related to epilepsy,
substance abuse and depression. Pharmacogenomics of anticonvulsant and antidepressant
drugs.RESEARCH TECHNIQUES
Animal models for seizures and drug abuse; Quantitative trait loci (QTL) and gene mapping; Single nucleotide polymorphism (SNP) analysis; Gene expression analysis; Congenic and transgenic miceRESEARCH SUMMARY
The general focus of my research program is on understanding the relationship between complex traits and genetic susceptibility to disorders of the central nervous system. Experiments are carried out first in animal models of human neurological and psychiatric disorders and eventually results are translated into clinical studies. Our basic approach starts with mapping and identifying (mouse) genes that influence the model phenotype. This is followed by examining those same genes in humans who exhibit homologous disease phenotypes.
A prime focus of my effort involves localizing and identifying genes that determine seizure susceptibility in models of epilepsy. Molecular studies examine natural gene variation in seizure sensitive and resistant strains of mice. Recently, we identified a genetic variation in a gene encoding an inward-rectifying potassium ion channel (Kcnj10) that is associated with differences in seizure threshold in mice. Following this, we showed that Kcnj10 is also a susceptibility factor for generalized idiopathic and temporal lobe epilepsy in humans. It is hoped that identification of this and other novel seizure-related genes will lead to new advances in understanding and treating epilepsy.
A number of experimental genetic models are also being studied in the
area of substance abuse. We recently mapped a gene that has a major role
in determining morphine preference in mice to the proximal region of chr
10. A provocative candidate gene in this region, the mu opioid receptor
gene, is being screened for sequence variation that could affect murine
opioid responsiveness. In a clinically-related study, variation in the
human mu opioid receptor gene is being analyzed using DNA from opioid-dependent
and control subjects again demonstrating how the strategy utilized in
our lab involves moving from 'bench to bedside'. Other genetic studies
in experimental animal models involve the mapping of genes influencing
alcohol- and cocaine-related phenotypes.
Another human genetic study in our lab is ongoing in the area of manic depression. Using linkage analysis and systematic genomic scanning, we generated evidence for the presence of a predisposing gene for bipolar disorder on the short arm of chromosome 18. Current work is focused upon screening a number of candidate genes from this region for causative genetic variation using case-control and related experimental designs.
KEY WORDS:
complex traits, behavioral genetics, quantitative trait loci (QTL), gene mapping, epilepsy, seizures, bipolar disease, substance abuse, neuropharmacology, pharmacogenetics, pharmacogenomics
