pete detloffAssociate Professor

Research Areas
molecular mechanisms of neurological disease


Peter J. Detloff (b. 1963) received his B.S. degree in Biochemistry from the University of Illinois at Champaign Urbana in 1985 and his Ph.D. degree from the University of Chicago in 1991. He was a postdoctoral fellow with Professor Oliver Smithies in the Department of Pathology in the School of Medicine at the University of North Carolina at Chapel Hill. In 1993 he joined UAB as an Assistant Professor in the Department of Biochemistry and Molecular Genetics.

Research Interests

The main goal of the Detlofflab is to understand the molecular mechanisms of neurological disease with the goal of finding molecular steps in the pathological processes that might be modulated to provide therapeutic benefit. Our focus has been on Huntington’s Disease, a late onsetneurological disease caused by the inheritance of an expanded CAG/polyglutamine repeat in a gene of unknown function called Huntingtin (HD). In order to provide an experimental system for the study of HD we engineered several HD knock-in mouse models. These mice exhibit HD-like features which are late onset and dependent on repeat length. Each line is available to the HD research community through the Jackson Laboratory.

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As in humans, mice with HD longer repeats tend to cause early onset of HD-like features. We developed an allelic series of knock-in HD mouse models that allows analyses of any potential molecular change across the series. Such analyses are useful in assessing the potential involvement of any altered molecular process in causing the HD-like features in these mouse lines. Our initial use of the allelic series revealed that of the thousands of mRNA levels that differ in the striatum (a brain area affected by HD) between normal and knock-in mice, only a handful correlated with the degree of phenotypic severity across the allelic series. Our current efforts are to deepen our initial analysis of the transcriptome, to extend this analysis to determine alterations in the proteome and metabolome while providing the field with bioinformatics coding resources allowing discorrelate analyses to be performed on this and other diseases.

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Our second major focus in the lab is to develop small molecules capable of downregulating expression of mutant HD alleles. We have found a process that when inhibited decreases the expression of expanded mutant HD mRNA levels in the brains of knock-in mice. The compounds we have currently do not cross the blood brain barrier, so we are performing a high throughput screen to find other inhibitors. The goal of this project is to develop a small molecule with good pharmacokinetic properties that could be used to delay or prevent the onset and progression of HD.


Graduate School
Ph.D., University of Chicago

Postdoctoral Fellowship
University of North Carolina at Chapel Hill


Kaul Human Genetics Building
Building Room 402C
720 20th Street South
Birmingham, AL 35233

(205) 975-8157