Pierre De Rossi PhD Neuroscience

Course and current status

12/2018 - today

Research associate in the Polymenidou group

University of Zurich

Zurich, Switzerland

Aim: Development of new models to study ALS and FTLD pathogenesis in vitro and in vivo


06/2014 – 11/2018

Post-doctoral Scholar in the Thinakaran lab

the University of Chicago

Chicago, IL, USA

Aim1: BIN1 physiological roles in the brain in myelination process and synaptic plasticity, learning and memory.

Aim2: BIN1 pathological implication in Amyloid pathology and/or Tau pathology 


01/2014 – 06/2014

Post-doctoral Fellow

Lyon Neuroscience Research Center

ONCOFLAM team (Neuro-oncology and neuro-inflammation)

Lyon, France

Aim: Elucidate the impact of auto-antibodies (limbic encephalitis) in synaptic remodeling, receptors internalization and trafficking and signaling pathway implicated.


Scientific summary

I am a neuroscientist specialized in cellular and molecular neurobiology. My goal is to develop a research team, which will focus on early mechanisms involved in neurodegenerative diseases and to explore possible common mechanism in neurodegeneration.

During my Ph.D., I worked on the regulation of synaptic plasticity and synaptogenesis by VEGF, a vascular growth factor, and its consequences on learning and memory. I demonstrated that VEGF regulates NMDAR and AMPAR synaptic localization and increases the number of synaptic sites when coupled with synaptic activity. Moreover, I found that VEGF can trigger specific pathways implicated in learning and memory, and that the deletion of VEGFR2 in animal models decreased learning capacities (De Rossi et al, 2016). After my Ph.D., I spent 6 months studying the effects of autoantibodies, implicated in limbic encephalitis, on the synaptic composition and signaling pathway regulation. I studied the effects of NMDAR antibodies on hippocampal functions (Mikasova et al, 2012) and mGluR1 antibodies role in cerebellar ataxia.

In 2014, I joined Pr. Gopal Thinakaran's lab at the University of Chicago to perform research on the cellular biology of Alzheimer disease. There, I was studying BIN1, a recently identified gene as a major genetic risk factor for late-onset Alzheimer’s disease. The first part of my work was to explore BIN1 expression in the brain (De Rossi et al, 2016, De Rossi et al, 2017), as very few studies have been investigating BIN1 precise localization before. My latest projects were focusing on BIN1 functions in the brain and cellular mechanisms in oligodendrocytes (ie myelination, survival, differentiation…), in neurons (learning and memory) and its dysregulation in Alzheimer’s disease. My work used complementary approaches of cellular biology (cell culture, transfection, trafficking and microscopy), molecular biology (plasmid design for in vitro interaction binding experiment and antibodies development) and animal models (behavior, IHC, IHF and biochemistry). Over the years, I have acquired experience in different microscopy techniques including STORM microscopy, 3D STED and confocal microscopy and I have experience in electron microscopy analyses. My last project uncovered a unique profile of BIN1 aggregation within the amyloid deposits in several mouse models for Alzheimer’s disease (De Rossi et al, 2018, Andrew et al, 2019). I have also characterized the presynaptic localization of BIN1 at excitatory synapses and uncovered a role for BIN1 in presynaptic release of glutamate and learning and memory (De Rossi et al, under revision). Before leaving the University of Chicago, I was finalizing a study demonstrating a role for BIN1 in the regulation of oligodendrocytes cytoskeleton organization and oligodendrocytes maturation. I was funded by the Alzheimer’s Association and the Brightfocus Foundation to explore the role of BIN1 in the seeding and propagation of Tau pathology in the brain.

In December 2018, I joined the Department of Quantitative BioMedicine (DQBM) at the University of Zurich (UZH). Here, I am working with Pr. Magdalini Polymenidou on developing a new mouse model to decipher cellular mechanisms of TDP-43 associated pathologies [Amyotrophic Lateral Sclerosis (ALS) and frontotemporal lobar degeneration (FTLD)]. My work is using iPSC-derived human neuronal culture, compartmentalized culture and inoculated mouse models. I will explore behavioral performance after stereotaxic injection of TDP-43 in the brain and I will follow the evolution of TDP-43 pathology in the brain using state-of-the-art in vivo imager IVIS Spectrum imager.

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