Researchers

Acting Group leader: Ilaria Bertocchi

Ilaria Bertocchi
Assistant Professor in Pharmacology
Alessandra Oberto
Assistant Professor in Pharmacology and Toxicology
Alessandra Lodi
Research Fellow

PhD Students

Lorenzo Cifarelli

 

Lorenzo Cifarelli joined NICO in 2019 as an undergraduate student in the Neuropsychopharmacology group. Here, during his Master degree, he contributed to the development of a novel bioinformatic approach for the automated analysis of perineuronal nets (PNNs) and parvalbumin-positive inhibitory interneurons (PVIs) ex vivo in a mouse model of fragile X syndrome (Fmr1KO mouse), the first genetic cause of autism spectrum disorders. In 2022 after Master graduation, in the S&P Brain startup, he conducted an in vivo preclinical testing of an antiepileptic drug in the GluN2A(N615S) murine model of developmental and epileptic encephalopathy (DEE). Then, during a period as a research fellow for the University of Turin’s Department of Neuroscience, he analyzed behavior and PNN expression in the Fmr1KO and GluN2A(N615S) models. At the end of 2023 he started his PhD in Experimental Medicine and Therapy, focusing on the study of PNNs to identify new therapeutic strategies for DEEs.

In the Neuropsychopharmacology group at NICO, Lorenzo Cifarelli is studying PNN expression and manipulation in two murine models of DEEs. In particular, he is focusing on the positive influence of a ketogenic diet on seizure susceptibility in the GluN2A(N615S) mice and its relation to PNN and PVI expression. In the Fmr1KO model he aims to produce a reference atlas for PNNs and PVIs, to help understand their role in the context of autism spectrum disorders. To investigate PNN and PVI expression in these models, he is making use of a novel bioinformatic workflow which he helped to develop. With this approach he found that ketogenic diet is able to alter PNN and PVI expression in the GluN2A(N615S) mice, whereas with a whole-brain analysis he showed that in the Fmr1KO brains PNNs are reduced compared to healthy counterparts. He recently presented these results at national and international congresses, such as the FENS (Federation of European Neuroscience Societies) forum.

 

Related News

The adaptor protein SKT interacts with PSD-95 and SHANK3 and affects synaptic functions

Cell Reports, September 2025 Highlights • SKT is a postsynaptic scaffold interacting directly with PSD95 and SHANK3 • SKT loss causes defects in dendritic spine formation, morphology, and maturation • SKT loss leads to a significant reduction in excitatory synaptic transmission • SKT-KO mice exhibit impaired motor, cognitive, and executive functions

Subscribe to our newsletter
Stay updated on news and projects

Subscribe to our newsletter
Stay updated on news and projects