Thesis project: Cocaine and Activity Dependent Neuroprotective Protein (ADNP)
Why is addiction so… addicting? Why is it so difficult to break an addiction, and so easy to relapse?
According to the 'pathological learning' model of addiction, drugs of abuse sustain their power by hijacking neural mechanisms that underlie reward-related learning and memory. In other words, drugs take over existing pathways in order to create stable and long-lasting memories. One way this occurs is through changes to the cell structure, including alterations in dendritic spines, the site of the synapse.
My research focuses on cocaine, a psychoactive drug, and activity-dependent neuroprotective protein (ADNP), an essential protein for brain development and maintenance. Its active fragment NAP (NAPVSIPQ) binds to microtubule end-binding (EB) proteins 1/3 and provides broad neuroprotection. NAP treatment decreases tau hyperphosphorylation, ameliorates cognitive and synaptic deficits associated with ADNP deficiency, and protects embryos against ethanol-induced neural tube defects.
Working in vitro, I use molecular and imaging techniques to study how cocaine damages the cell cytoskeleton, and the mechanisms through which ADNP and its active fragment, NAP, might protect against this damage.
By characterizing drug effects at the cellular level, I hope to contribute to one piece of the puzzle surrounding drugs, brain, and ourselves.