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Elisabetta Battocchio

Elisabetta Battocchio

Curriculum vitae

Nata l’11 Novembre 1994, ha conseguito la Laurea Magistrale a ciclo unico in Farmacia e Farmacia Industriale nel 2019 presso l’Università degli Studi di Milano. Ha svolto il tirocinio sperimentale per la tesi finale dal titolo “Interazione diretta tra β-amiloide e proteina Tau ed effetti sulla formazione di fibrille amiloidi” presso l’Istituto di Ricerche Farmacologiche “Mario Negri” nel laboratorio di Farmacodinamica e Farmacocinetica del Dr Marco Gobbi.

Questo periodo le ha permesso di apprendere la tecnica di Surface Plasmon Resonance (SPR) e le sue applicazioni in diversi ambiti, ma anche tecniche base di biologia molecolare e analisi di cinetiche di aggregazione con ThT assay.

Nel 2019 ha vinto una borsa di studio presso l’Università degli Studi di Milano Bicocca per il progetto “Caratterizzazione degli autoanticorpi anti-Amiloide monomerica versus oligomerica mediante Risonanza Plasmonica di Superficie nel CSF di pazienti affetti da angiopatia amiloide cerebrale infiammatoria” presso il laboratorio CAA and AD Translational Research and Biomarkers del Dr Fabrizio Piazza, diventando membro dell’Inflammatory Cerebral Amyloid Angiopathy and Alzheimer’s Disease Biomarkers (iCAB) International Network.

Da novembre 2020 è dottoranda in Neuroscienze sperimentali presso l’Università degli Studi di Milano Bicocca, in collaborazione con l’Istituto di Neuroscienze del Centro Nazionale delle Ricerche. Sta svolgendo la sua attività presso il laboratorio Cell-to cell signaling in brain sotto la supervisione della Dr.ssa Claudia Verderio e del Prof Giulio Alfredo Sancini.

PhD Project

Exploring molecular interactors mediating motion of glial extracellular vescicles (EVs) carrying pathogenic misfolded proteins at the neuron surface

  • Curriculum: Neuroscienze sperimentali
  • Tutor: Prof. Giulio Alfredo Sancini   Cotutor: Dr.ssa Claudia Verderio

Extracellular vesicles (EVs) are circular membrane fragments which function as intercellular signalling vehicles. They transfer bioactive cargoes influencing both the behaviour of the target cells and the surrounding environment.

In the brain, accumulating evidences indicates that glial cells communicate with neurons through secretion of EVs and in the diseased brain EVs become vehicle of pathogenic molecules, including misfolded proteins, such as β-amyloid and Tau protein, associated with neurodegeneration. Moreover, data from the lab I am working in show that microglial large EVs (>200 nm in diameter) carrying Aβ efficiently move extracellularly along axonal processes spreading synaptic dysfunctions in the mouse brain. In addition, EVs isolated from CSF of AD patients have been found to propagate tau pathology after injection in mouse brain.

The aim of my PhD project is to investigate the molecular mechanisms underlying large EV extracellular motion at the neuron surface.

To do this, three different aspects will be investigated: i) proteomic analysis of surface proteins in EVs released from microglia exposed to Aβ and/or Tau protein, ii) analysis of estracellular motion of these EVs on neurons lacking candidate EV receptors and iii) analysis of the impact of these EVs on dendritic spine morphology.

Primary cultures of neurons and microglia will be used and optical manipulation experiments combined with time-lapse imaging will be employed in order to study EV-neuron interaction dynamics and EV effects on dendritic spine morphology after placing single EVs in contact with the neuronal surface. Finally, neurons lacking candidate receptors for the EVs will be used in order to investigate the binding partners of EVs on neurons surface.

Hopefully this study will pave the way to novel therapeutic strategies to limit the spreading of synaptic dysfunciton and neurodegenerative processes in Alzheimers’ Disease.

Congressi e workshop

  • SINdem 2020 – Firenze, 12-14 marzo 2020
  • Alzheimer’s Association International Conference 2020 – 26-30 luglio 2020
  • Congresso Scientifico Annuale AISM 2020 – 27 novembre 2020
  • NeuroMI 2020 virtual annual meeting – 18 dicembre 2020

Pubblicazioni

  • Beeg, M., Battocchio, E., et al. (2021). Nonphosphorylated tau slows down Aβ1-42 aggregation, binds to Aβ1-42 oligomers, and reduces Aβ1-42 toxicity. Journal of Biological Chemistry, 296(15), 100664. https://doi.org/10.1016/j.jbc.2021.100664

Altre informazioni

Elisabetta Donzelli
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