Tara Tracy, PhD

I received my bachelor’s degree in biology and neuroscience at Wesleyan University. In 2004, I began my graduate training in the Helen Wills Neuroscience Institute at the University of California, Berkeley. Under the mentorship of Lu Chen, PhD, I studied the role of AMPA-type glutamate receptors in synapse development. For my postdoctoral work, I wanted to apply my knowledge of synapse biology to research on neurodegenerative disease. In 2011, I joined the laboratory of Li Gan, PhD, at the Gladstone Institute of Neurological Disease, for my postdoctoral training. We found that an increase in the acetylation of two lysine residues on tau, K274 and K281, is associated with severe dementia in AD. Using transgenic mice expressing tau mutated to mimic K274 and K281 acetylation, we showed that acetylated tau inhibits hippocampal synaptic plasticity and causes AD-related memory impairments. At synapses, acetylated tau blocks the actin cytoskeleton remodeling and glutamate receptor recruitment required for long-term synaptic strengthening. We found that this plasticity deficit involves a reduction in KIBRA levels at synapses, and we are continuing to investigate how the loss of KIBRA contributes to memory loss in AD.