Aislinn Williams, MD, PhD

Portrait
Assistant Professor of Psychiatry

Contact Information

Primary Office
2326 PBDB
319-335-2434

Education

BA, Neuroscience, Smith College
MD, University of Iowa Carver College of Medicine
PhD, Neuroscience, University of Iowa
Resident, Adult Psychiatry, University of Michigan
Postdoctoral Scholar, Psychiatry, University of Michigan

Licensure and Certifications

Board Certified in General Psychiatry - ABPN

Education/Training Program Affiliations

Interdisciplinary Graduate Program in Neuroscience

Center, Program and Institute Affiliations

Iowa Neuroscience Institute

Research Summary

The Williams lab is interested in understanding the molecular and cellular mechanisms by which genetic risk factors contribute to psychiatric disease from a developmental perspective. Our current projects focus on voltage-gated calcium channel genes, which have been linked to the risk of developing bipolar disorder, schizophrenia, depression, and autism. We use induced pluripotent stem cells and transgenic mouse models to study how calcium channel gene SNPs alter neuronal development, neural circuit function, and affective behavior. We employ a wide range of approaches, including molecular biology, live cell imaging, neuropathology, and animal behavioral assessments, to try to unravel the developmental pathways involved in neuropsychiatric disease, in the hope of identifying novel treatment targets.

Publications

Williams, A. J., Wang, Z. & Taylor, S. F. (2016). Atypical psychotic symptoms and Dandy-Walker Variant. (Vols. 23). pp. 1-4. Neurocase. DOI: 10.1080/13554794.2016.1237657.

Williams, A. J., Yee, P., Smith, M. C., Murphy, G. G. & Umemori, H. (2016). Deletion of Fibroblast Growth Factor 22 (FGF22) causes a depression-like phenotype in adult mice. BehavBrain Res, 307, 11-17.

Williams, A. J., Umemori, H. (2014). The best laid plans go oft awry: synaptogenic growth factor signaling in neuropsychiatric disease. Front. Synaptic Neurosci., 6, 4.

Seki, T., Gong, L., Williams, A. J., Sakai, N., Todi, S. V. & Paulson, H. L. (2013). JosD1, a membrane-targeted deubiquitinating enzyme, is activated by ubiquitination and regulates membrane dynamics, cell motility and endocytosis. (Vols. 288). pp. 17145-17155. J. Biol. Chem.

Durcan, T. M., Kontogiannea, M., Thorarinsdottir, T., Fallon, L., Williams, A. J., Djarmati, A., Fantaneanu, T., Paulson, H. L. & Fon, E. A. (2011). The Machado-Joseph disease-associated mutant form of ataxin-3 regulates parkin ubiquitination and stability. Hum Mol Genet, 20, 141-154.

Williams, A. J., Knutson, T. <., Colomer Gould, V. F. & Paulson, H. L. (2009). In vivo suppression of polyglutamine neurotoxicity by C-terminus of Hsp70 interacting protein (CHIP) supports an aggregation model of pathogenesis. Neurobiol. Dis., 33, 342-353.

Williams, A. J., Lai, Z., Knight, S., Kamali, M., Assari, S. & McInnis, M. G. (2018). Risk Factors Associated With Antidepressant Exposure and History of Antidepressant-Induced Mania in Bipolar Disorder. The Journal of clinical psychiatry, 79(3). PMID: 29873955.

Williams, A. J. (2008). Polyglutamine neurodegeneration: protein refolding revisited. Trends Neurosci, 31, 521-528.

Winborn, B. J., Travis, S. M., Todi, S. V., Scaglione, K. M., Xu, P., Williams, A. J., Cohen, R. E., Peng, J. & Paulson, H. L. (2008). SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model. J Clin Invest, 118, 659-670.

Harraz, M. M., Marden, J. J., Zhou, W., Zhang, Y., Williams, A., Sharov, V. S., Nelson, K., Luo, M., Paulson, H., Schöneich, C. & Engelhardt, J. F. (2008). SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model. J Clin Invest, 118, 659-670.

Todi, S. V., Winborn, B. J., Williams, A. J. & Paulsen, H. L. (2008). Ubiquitination of the polyglutamine disease protein ataxin-3 enhances its activity as a deubiquitinating enzyme. (Vols. 22). pp. 1026. FASEB J.

Todi, S. V., Williams, A. J. & Paulson, H. L. (2007). Polyglutamine Repeat Disorders, including Huntington’s Disease. In S. G. Waxman (Eds.) Molecular Neurology. pp. 257-276. Academic Press.

Marden, J. J., Harraz, M. M., Williams, A. J., Nelson, K., Luo, M., Paulson, H. & Engelhardt, J. F. (2007). Redox modifier genes in amyotrophic lateral sclerosis in mice. J Clin Invest, 117, 2913-2919.

Williams, A. J., Knutson, T. M., Colomer Gould, V. F., Osmand, A. P. & Paulson, H. L. (2006). Suppression of polyglutamine neurotoxicity by C-terminus of Hsp70 interacting protein (CHIP) supports an aggregation model for polyglutamine disease pathogenesis. (Vols. 22). pp. V. Movement Disorders.

Miller, V. M., Nelson, R. F., Gouvion, C. M., Williams, A., Rodriguez-Lebron, E., Harper, S. Q., Davidson, B. L., Rebagliati, M. R. & Paulson, H. L. (2005). CHIP suppresses polyglutamine aggregation and toxicity in vitro and in vivo. J. Neurosci, 25, 9152-9161.

Powell, J. A., Molgo, J., Adams, D. S., Colasante, C., Williams, A., Bohlen, M. & Jaimovich, E. (2003). IP3 receptors and associated Ca2+ signals localize to satellite cells and to components of the neuromuscular junction in skeletal muscle. J. Neurosci, 23, 8185-8192.

Chai, Y., Shao, J., Miller, V. M., Williams, A. & Paulson, H. L. (2002). Live-cell imaging reveals divergent intracellular dynamics of polyglutamine disease proteins and supports a sequestration model of pathogenesis. Proc Natl Acad Sci U S A, 99, 9310-9315.

Powell, J. A., Adams, D. S., Molgo, J., Colasante, C., Williams, A., Bohlen, M. K. & Jaimovich, E. (2001). IP3 receptor function and localization in skeletal muscle in vitro and in vivo: A new calcium signaling pathway in muscle. (Vols. 34). pp. R-9. Biol Res.

Williams, A., Frost, R. (2000). Body Dysmorphic Disorder and Perfectionism in a Nonclinical Sample. In Women in Science: 1999 Summer Student Research. Clark Science Center, Smith College.

Williams, A., McInnis, M. G. Sex differences in the incidence of antidepressant-induced mania (AIM) in bipolar disorders. Neuropsychopharmacology. DOI: 10.1038/s41386-018-0216-4.