The overall goal of my research is to understand the basic mechanisms underlying neural specification and maturation, and how those processes go awry in disorders that cause intellectual disability (ID). Our lab currently focuses on the modeling neural development using a combination of rodent systems both in vitro and in vivo, as well as human pluripotent stem cell-derived neurons (hPSNs). We employ a range of techniques including viral vector engineering, optogenetics, CRISP/cas9 gene editing, electrophysiology as well as timelapse and super-resolution microscopy. Using these techniques we have uncovered novel proteins and pathways that lie at the heart of neuronal differentiation and functional maturation and are currently using this knowledge to develop novel ways to model ID both in vitro using hPSNs as well as in vivo rodent models.

Areas of Specialty

Alzheimer’s Disease


Post-Doc (2009):
University of Wisconsin-Madison
Phd (2005):
University of Minnesota-Twin Cities
BS (200):
Denison University 2000

Achievements & Awards

Selected as Lead Guest Editor: Special Issue of Stem Cells International - 2016
Weick et al., 2011 (PNAS) selected by ‘Faculty of 1000’ as part of the top 2% of publications - 2011
Wisconsin Stem Cell Research Symposium Award - 2006




  • English

Research and Scholarship

Work in the Weick lab centers on understanding multiple aspects of the development of functional neural circuits, from how individual neurons acquire functional properties to how groups of neurons generate patterns of information. Using neurons differentiated from pluripotent stem cells we study development both under normal conditions and in the context of developmental disorders. One of our basic science projects focuses on the Neuron-Specific Gene (NSG) family of proteins, which aid in the shuttling of AMPA receptors within post-synaptic compartments to regulate synaptic plasticity. We recently discovered that NSG proteins appear to play unique roles in shaping synaptic strength, and possibly defining unique sets of post-synaptic densities. We are also examining their role in Alzheimer’s disease, as NSG proteins form complexes with the Sortilin-1 receptor, which is an APOE receptor that is critical for regulating the levels of intra and extracellular APOE. Furthermore, we are investigating the effects of ethanol on developing neurons during early stages of synapse formation, using a newly developed technique to map the SYNAPTOME of mice. We hypothesize that early insults of fetal alcohol exposure will cause significant remapping events that cause underlying functional and behavioral pathology.