Experience

Dewpoint Therapeutics

• United States
• Biotechnology Research
• 100 - 200 Employee

• Senior Scientist

  • Oct 2022 - Present

  Boston, Massachusetts, United States



Vesalius Therapeutics

• United States
• Biotechnology Research
• 1 - 100 Employee

• Scientist II

  • Mar 2022 - Sep 2022

  Cambridge, Massachusetts, United States •Designed and executed cell-based assays for target validation for a neurodegenerative disease indication •Drove the successful nomination of a target and led the cross-functional program for a neurodegenerative disease indication based on the proprietary Vesalius Diamond platform •Effectively managed CRO project to supplement in-house capabilities •Involved in departmental goal-setting, delivery, and strategic planning •Regularly presented results at Discovery Biology, project… Show more •Designed and executed cell-based assays for target validation for a neurodegenerative disease indication •Drove the successful nomination of a target and led the cross-functional program for a neurodegenerative disease indication based on the proprietary Vesalius Diamond platform •Effectively managed CRO project to supplement in-house capabilities •Involved in departmental goal-setting, delivery, and strategic planning •Regularly presented results at Discovery Biology, project team, and all-company meetings •Managed two direct reports

• Scientist I

  • Jun 2021 - Mar 2022

  Cambridge, Massachusetts, United States •Developed and optimized 2D and 3D iPSC-derived models •Implemented differentiation quality control metrics for iPSC-derived cultures •Successfully drove the parallel culturing, differentiation, and phenotypic profiling (using cell-based and biochemical readouts) of patient-derived iPSC lines to support platform and target validation efforts



Brigham and Women's Hospital

• Hospitals and Health Care
• 700 & Above Employee

• Postdoctoral Fellow

  • Jun 2015 - Jun 2021

  Boston, Massachusetts, United States •Principal investigator of 5 year NIH K22 grant •Examined neurodegenerative features of Christianson syndrome (CS), a disease caused by loss of function of the endosomal exchanger NHE6, using iPSC-derived neurons •Discovered pathological changes in tau protein in iPSC-derived CS neurons, including elevated levels of insoluble and phosphorylated tau •Gained mechanistic insight into the elevated phospho-tau phenotype in CS neurons by demonstrating partial rescue by an enhancer of… Show more •Principal investigator of 5 year NIH K22 grant •Examined neurodegenerative features of Christianson syndrome (CS), a disease caused by loss of function of the endosomal exchanger NHE6, using iPSC-derived neurons •Discovered pathological changes in tau protein in iPSC-derived CS neurons, including elevated levels of insoluble and phosphorylated tau •Gained mechanistic insight into the elevated phospho-tau phenotype in CS neurons by demonstrating partial rescue by an enhancer of autophagy-lysosomal function •Optimized the acquisition and analysis of high content imaging data and used these methods to discover altered endosome and lysosome number and size in CS neurons •Developed functional assays to characterize autophagy-lysosomal activity and determined that CS neurons exhibit reduced lysosomal protease activity and autophagic dysfunction •Contributed to projects analyzing tau biochemistry in various sporadic and familial Alzheimer’s disease iPSC models Show less



Harvard Medical School

• United States
• Higher Education
• 700 & Above Employee

• Doctoral Student

  • Sep 2009 - May 2015

  Boston, Massachusetts, United States •Characterized the C-terminal trimming function of the protease γ-secretase in vitro and in cells •Determined that familial Alzheimer’s disease-causing mutations in γ-secretase dramatically reduce the catalytic efficiency of this carboxypeptidase activity •Investigated substrate determinants for γ-secretase processing of the amyloid precursor protein, demonstrating that substrate amino acid sequence determines the initial γ-secretase cleavage site, and that substrate helical… Show more •Characterized the C-terminal trimming function of the protease γ-secretase in vitro and in cells •Determined that familial Alzheimer’s disease-causing mutations in γ-secretase dramatically reduce the catalytic efficiency of this carboxypeptidase activity •Investigated substrate determinants for γ-secretase processing of the amyloid precursor protein, demonstrating that substrate amino acid sequence determines the initial γ-secretase cleavage site, and that substrate helical instability is crucial for carboxypeptidase cleavage by γ-secretase Show less