“While working as a senior scientist in the lab of Drs. Virginia Lee and John Trojanowski at the University of Pennsylvania, Dr. Volpicelli-Daley discovered that fibrils of α-synuclein act as seeds to template the growth of α-synuclein inclusions from endogenously expressed α-synuclein in neurons. These inclusions are remarkably similar morphologically and biochemically to those found in PD. Importantly, she showed the fibrils do not cause phenotypes in neurons lacking endogenous α-synuclein,
demonstrating that corruption of normal α-synuclein contributes to neuronal defects. Currently, her lab focuses on the impact of pathologic α-synuclein on synapse architecture and function in the cortex and limbic brain regions. In addition, the lab studies how accumulation of glycosphingolipids in the brain causes neuronal dysfunction, synapse loss, and cognitive decline in PD.
Lead PI (Core Leadership)
Laura Volpicelli-Daley, PhD
University of Alabama at Birmingham
“While working as a senior scientist in the lab of Drs. Virginia Lee and John Trojanowski at the University of Pennsylvania, Dr. Volpicelli-Daley discovered that fibrils of α-synuclein act as seeds to template the growth of α-synuclein inclusions from endogenously expressed α-synuclein in neurons. These inclusions are remarkably similar morphologically and biochemically to those found in PD. Importantly, she showed the fibrils do not cause phenotypes in neurons lacking endogenous α-synuclein,
demonstrating that corruption of normal α-synuclein contributes to neuronal defects. Currently, her lab focuses on the impact of pathologic α-synuclein on synapse architecture and function in the cortex and limbic brain regions. In addition, the lab studies how accumulation of glycosphingolipids in the brain causes neuronal dysfunction, synapse loss, and cognitive decline in PD.
