• Title Postdoctoral Associate
  • Education PhD in neuroscience, International School for Advanced Studies,Trieste, Italy
  • Office Harris laboratory, K206
  • Area of Interest Neuroscience, Alzheimer’s disease and Prion diseases

My main research focuses on cellular neuroscience and I am particularly interested in studying the molecular and cellular mechanism underlying neurodegenerative diseases. During my scientific career, I received broad academic training and my research interest shifted from physics to neuroscience. This interdisciplinary background enabled me to apply the latest developments in nanotechnology and imaging to neuroscience.

I received my PhD in neuroscience from International school for advanced studies (Dr. Torre’ laboratory, SISSA, Trieste, Italy). My doctoral research project aimed at unraveling the molecular mechanisms underlying the force generation in neuronal growth cones. To address this issue, I have investigated in detail the role of several important players in force generation such as membrane stiffness, actin turnover and myosin II. After PhD, I was involved in different research projects related to protein misfolding and prion diseases in collaboration with Dr. Legname and Dr. Cojoc (SISSA, Trieste, Italy). My main research project was focused on defining the physiological function of prion protein (PrPC) by analyzing its role on neurite guidance and signaling.

In order to extend my knowledge in the neurodegeneration field, I joined Dr. Harris’ Laboratory. I am particularly excited about this opportunity, which will complement my previous training by introducing me to the field of Alzheimer’s disease and will help me to learn new skills in protein chemistry and cell biology. Currently, my research project focuses on identifying the molecular mechanism by which amyloid-β (Aβ) aggregates interact with cell surface receptors including PrPC. In this work, I am using a multi-disciplinary approach combining single molecule super-resolution microscopy, biochemical and biophysical assays, and cell-based neurotoxicity experiments to measure the dynamics and kinetics of Aβ interactions with its membrane receptors. Analyzing several Aβ-receptor systems in parallel will reveal common molecular mechanisms by which receptors interact with pathologically relevant Aβ aggregates to transduce neurotoxic signals. I believe, this study will provide deep insights into a molecular origin of disease, and the development of therapeutic approaches for Alzheimer’s disease.

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