Aaron Bowman, Ph.D.

Assistant Professor

Phone: (615) 322-2651
Fax:
Email: aaron.bowman@vanderbilt.edu

Affiliations

My lab utilizes a combined approach of molecular genetics, biochemistry, cell and developmental biology to understand the gene-environment interactions underlying neurodegenerative diseases. We employ a diverse range of model systems including patient-derived induced pluripotent stem cells (iPSCs), neuronal culture and mouse models of Huntington's disease, Down syndrome/Alzheimer's disease and other diseases. We aim to define mechanisms of neuronal dysfunction and understand the basis of selective neuropathology, by characterizing the molecular function of disease genes and their interaction with environmental agents under both normal and pathological conditions. We are primarily studying interactions between metal and other toxicant exposures and neurodegenerative disease states.

Publications

PubMedID	Citation
18337722	Lim J, Crespo-Barreto J, Jafar-Nejad P, Bowman AB, Richman R, Hill DE, Orr HT, Zoghbi HY. Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1. (2008) Nature 452: 713-8
17322884	Bowman AB, Lam YC, Jafar-Nejad P, Chen HK, Richman R, Samaco RC, Fryer JD, Kahle JJ, Orr HT, Zoghbi HY. Duplication of Atxn1l suppresses SCA1 neuropathology by decreasing incorporation of polyglutamine-expanded ataxin-1 into native complexes. (2007) Nat Genet 39: 373-9
17190598	Lam YC, Bowman AB, Jafar-Nejad P, Lim J, Richman R, Fryer JD, Hyun ED, Duvick LA, Orr HT, Botas J, Zoghbi HY. ATAXIN-1 interacts with the repressor Capicua in its native complex to cause SCA1 neuropathology. () Cell 127: 1335-47
16494529	Helmlinger D, Hardy S, Abou-Sleymane G, Eberlin A, Bowman AB, Gansmüller A, Picaud S, Zoghbi HY, Trottier Y, Tora L, Devys D. Glutamine-expanded ataxin-7 alters TFTC/STAGA recruitment and chromatin structure leading to photoreceptor dysfunction. (2006) PLoS Biol 4: e67
15661755	Bowman AB, Yoo SY, Dantuma NP, Zoghbi HY. Neuronal dysfunction in a polyglutamine disease model occurs in the absence of ubiquitin-proteasome system impairment and inversely correlates with the degree of nuclear inclusion formation. (2005) Hum Mol Genet 14: 679-91