Born in Benevento, on February 14, 1995; in March 2020 she obtained the Master’s Degree in Molecular and Cellular Biology (LM-6) at the Alma Mater Studiorum of Bologna with a thesis focused on the study of alterations of histone acetylation in the proliferation and differentiation of oligodendrocyte precursors in an in vitro models of AGC1-deficiency.
Since November 2020 she is PhD student in Neuroscience at the University of Milano-Bicocca, carrying out her research activity at the “Rita Levi Montalcini” Neuroscience laboratory of Prof. Anna Maria Colangelo. The goal of the research is to investigate the crosstalk between mitochondrial dysfunction and neuroinflammation in mouse models of Parkinson disease.
Mechanisms linking mitochondrial dysfunction and neuroinflammation in mice models of Parkinson’s disease
- Curriculum: Neuroscienze Sperimentali
- Tutor: Anna Maria Colangelo
Parkinson’s disease is characterized by a progressive degeneration of nigrostriatal system with loss of dopaminergic neurons in Substantia nigra. Genetic and environmental factors linked to onset of PD converge on oxidative stress and mitochondrial dysfunction. Indeed, genes such as PTEN-induced kinase-1 (PINK1) and Parkin, which are related to some familiar forms of PD, are involved in mitochondrial quality control and regulation of mitochondrial morphology. On the other hand, several studies showed the relevance of neuroinflammatory processes and astroglial dysfunction. Nonetheless, little is known about mechanisms linking oxidative stress and alteration of neuroglial network underlying neuroinflammatory mechanisms in models of PD.
The aim of the project is to investigate the crosstalk between mitochondrial dysfunction and neuroinflammation in models of Parkinson’s disease. In particular, the project will focus on molecular events controlling mitochondrial dynamics in neuron and activated astrocytes and the mechanisms underlying the dysfunction of neuro-glial networks.
The study employ in vivo and in vitro models of PD based on the neurotoxin 6-hydroxydopamine (6-OHDA).
In vivo: mice (2moths old) treated with a single unilateral stereotaxic injection of 6-OHDA in the basal ganglia to produce a side-biased motor impairment. Mice are observed daily for motor behaviour and sacrificed at different times to evaluate both acute and chronic damage. Brain sections are used for immunohistochemical analysis of microglial/astrocytic activation and mitochondrial/metabolic machineries.
In vitro: primary cultures of neurons and astrocytes are used for detailed characterization of mitochondrial dysfunction by assessing mitochondria dynamic and morphology, bioenergetics, and neuronal/astrocytic metabolism.
Conferences and congresses
- European Neuroscience Conference by Doctoral Students (ENCODS) 2021, on 4-6th June