•Collaborative Lab Project: Optimizing the protein expression within three SOD (Superoxide dismutase) mutations; specifically the CTRØ G37A, G93A, and WT SOD protein variations. Mutations within the SOD protein are the principal causes of ALS, also known as Lou Gehrig’s disease, in humans. Research mentor: Dr. David Borchelt•Individual Project: Intended to inhibit or eliminate HSBP1 to allow HSF1 to effectively trigger a protein cascade required to produce a robust heath shock response in neurons. The primary objective is to test whether an effective Hsp40/Hsp70 response in neurons can be produced by modifying the level of HSBP1 expression. If successful, we believe we can unlock the full potential of the HSR within neurons and contribute to treatments of neurodegenerative diseases.Principal Investigator: Dr. David Borchelt•Lab Skills:Digestions, mini-preparations, immunostaining, western blots, transfections, maintaining neuronal and cell cultures, utilizing microscopes and cell imaging technologies, cloning, AAV vector creation.