Research Interests
Alzheimer’s Disease, Cadherins, Cell Adhesion Molecules, Cell Signalling, Confocal Imaging, Growth Factors, Learning and Memory, Nervous System Development, Neuronal Communication, Neurotransmission
Research Focus Teams
Autism, Alzheimer’s
Departments
Cellular and Physiological Sciences
Contact
Email: shernaz.bamji[at]ubc.ca
Office Phone: 604-822-4746
Office number: 2402, 2404, 2431
Publications
Lab Website
Dr. Shernaz Bamji is associate director of the Djavad Mowafaghian Centre for Brain Health and a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia. She is also the current president of the Canadian Association for Neuroscience.
Dr. Bamji has a long-standing interest in understanding the molecular and cellular mechanisms underlying neural connectivity and synaptic plasticity. Her work has provided valuable information about fundamental mechanisms underlying learning and memory, as well as how these processes are perturbed in diseased states.
Awards
2007/7 – 2012/7 New Investigator
Canadian Institutes of Health Research
2006/7 – 2012/7 Career Investigator Award
Michael Smith Foundation for Health Research
2005/10 – 2010/10 Salary Award, TULA Foundation
Research Goals:
- To understand the molecular mechanisms by which synaptic connections in the brain are formed, remodeled and eliminated;
- To determine how disruptions in the formation and/or plasticity of synaptic connections perturb brain function;
- To determine whether restoring synaptic function in the diseased brain can normalize cognitive and functional abilities.
Synapses of the central nervous system are highly specialized regions of cell-cell contact designed to rapidly and efficiently relay signals from one neuron to another. By establishing a dynamic yet precise network of synaptic connections, the brain is able to attain a level of functional complexity that enables not only simple motor tasks, but also sophisticated emotional and cognitive behaviour. The study of how synapses form and function is therefore essential to our ultimate understanding of higher brain functions such as learning and memory as well as our understanding of how things go awry in neurodevelopmental and neurodegenerative disorders such as intellectual disabilities, schizophrenia, autism, anxiety disorders, addiction and Alzheimer’s disease.
How do palmitoylating enzymes regulate synaptic connectivity and learning?
Our work demonstrates that DHHC enzymes, which mediate the posttranslational palmitoylation of proteins, are master regulatory ‘hubs’ for activity-dependent structural and functional plasticity critical to proper circuit formation (Nat Neurosci, 2014; Nat Commun, 2015). Building on these findings, we are currently exploring the roles of these enzymes in regulating synapse formation and plasticity, cognition and behavior. This is exceedingly important as 9 of the 23 DHHC enzymes have been linked to neurological disorders thus far and ~41% of all synaptic proteins are substrates for palmitoylation. We are one of a few labs worldwide studying this fundamental process in the brain.
How do adhesion complexes regulate synaptic connectivity and learning?
Our lab has demonstrated a role for cadherin adhesion complexes in synapse formation and plasticity, as well as cognition and behavior. Most recently, we demonstrated that increased cadherin-based adhesion at synapses of the reward circuit can block drug-seeking behaviors associated with addiction (Nat Neurosci, 2017). This study was an extension of our previous work elucidating molecular mechanisms underlying synapse formation (Neuron, 2003; J Biol Chem, 2008; Mol Cell Biol, 2009; J Biol Chem, 2010; Neurosci, 2010; J Neurosci, 2011), as well as our work demonstrating that cadherins promote synapse formation and plasticity in vivo (Neuron, 2003; PNAS, 2014).