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Bio

Francesco Limone, PhD

2025 Leon Levy Scholar in Neuroscience

NYU Grossman School of Medicine, Institute of Translation Neuroscience

Sub-disciplinary Category

Cellular & Molecular Neuroscience

Previous Positions

  • BSc, University of York
  • MS, University Pierre and Marie Curie
  • PhD, Harvard University (Dr. Kevin Eggan)

Bio

Dr. Francesco Limone is currently a postdoctoral fellow in Ass. Prof. Shane Liddelow’s lab at the Institute for Translational Neuroscience NYU Grossman School of Medicine. Their research focuses on expanding our knowledge on how neuron and astrocyte crosstalk is disrupted in disease. Originally from Central Italy, Francesco obtained a BSc in Molecular Cell Biology at the University of York (UK) and a Masters in Developmental and Stem Cell Biology at University Pierre and Marie Curie (UPMC, Paris VI – France). Francesco then expanded their knowledge in Molecular and Stem Cell Biology during their PhD in Kevin Eggan’s lab at the Harvard Stem Cell and Regenerative Biology Department with the goal to understand how inflammation contributes to neuronal death in Amyotrophic Lateral Sclerosis (ALS) using Pluripotent Stem Cells and animal models.

Research Summary

Understanding the disruption of healthy neuron-astrocyte communication in disease.

Technical Overview

Neurodegenerative diseases afflict the brain of aging populations and are becoming more and more relevant in our society. These disorders are usually the results of death of an important cell type of the brain called the neuron, followed by tissue degeneration and loss of brain function. Other cell types are also involved in a complex set of damage responses especially from neuron’s main support cells: astrocytes. Astrocytes are the most abundant non-neuronal brain cell, participate in neuronal functions and are the main providers of neurotrophic support. In disease, astrocytes respond to pro-inflammatory stimuli from microglia, the brain immune cells, and they lose physiologically supportive functions and acquire a neurotoxic reactive state. At present, not much is known about how many of these toxic reactive phenotypes are triggered by immune, pro-inflammatory stimuli and how many result from the disruption of the intrinsic, healthy neuron-astrocyte crosstalk. Francesco’s project will provide insights on how neuronal death independently contributes to loss of neurotropism and acquisition of neurotoxic states in astrocytes. It will also name targets to modulate astrocytic function that could support neuronal survival. Francesco wants to understand the interaction between dying neurons and astrocytes in order to find possible therapeutic avenues for neurodegenerative diseases.