POST-DOCTORAL FELLOWSHIP – TYPE A, 2022 I° CALL
POST-DOCTORAL FELLOWSHIP - TYPE A, 2022 I° CALL
First call for post-doc type A fellowship 2022 published on 27/05/2022, dead line for submission june 30 TH 2022 at noon (Italian time). Link al Bando [Assegni di ricerca | Università degli Studi di Milano Statale (unimi.it)]
Research lines suggested by the Department within the NEUROSCIENCE area:
1) Paola Riva (https://www.unimi.it/it/ugov/person/paola-riva )
We are carrying out a study aimed at identifying variants of RAS pathway genes possibly associated to cognitive impairment or learning disabilities, in patients with Noonan Syndrome or Neurofibromatosis type 1. We foresee to perform a functional validation of the identified variants by specific assays allowing to analyze possible biological changes in neuronal cellular and animal models, where the mutation can be expressed or the gene under study can be silenced.
2) Nicoletta Landsberger https://www.unimi.it/it/ugov/person/nicoletta-landsberger
Neural progenitor cell therapy: a novel therapeutic approach for the treatment of CDKL5 deficiency disorder? CDKL5 mutations are responsible for the CDKL5 deficiency disorder (CDD) a severe neurodevelopmental disorder characterized by the onset of early intractable seizures and severe intellectual disability. No cure exists and medical management is only symptomatic. Among advanced therapy medicinal products, adult stem cell-based approach has been extensively studied for neurodegenerative diseases, but little is known regarding their potential for neurodevelopmental disorders. Through in vitro and in vivo experimental approaches, we will investigate whether adult stem cells can improve neurological symptoms and neurobiological alterations typical of CDD and which are the molecular mechanisms involved in the potential beneficial effects.
3) Alessandro Prinetti https://www.unimi.it/it/ugov/person/alessandro-prinetti
This project is aimed at understanding the role of sphingolipids in myelin formation and stability, in particular, in relations with the mechanisms of myelin repair in demyelinating diseases.
In this sense, importance of the catabolic enzyme galactocerebrosidase (GALC) has been recently recognized. Carriers of GALC variants are at risk to develop multiple sclerosis (MS), due to impaired microglia function and defective myelin repair, and our preliminary data suggest that GALC expression is important for oligodendrocyte maturation and increased upon myelin-repairing treatments. On this basis, aims of the project are:
1) to elucidate the role of GALC in the formation, maintenance and stability of myelin;
2) to understand the molecular mechanisms linking GALC mutations with increased MS risk;
3) to explore GALC as a possible therapeutic target for MS treatment.
4) Flavia Antonucci https://www.unimi.it/it/ugov/person/flavia-antonucci
ATM and ATR in neuronal functions: beyond the DNA damage. The Unit headed by Prof. Flavia Antonucci refers to neurodevelopmental disorders. In lab it has been studying the new role of proteins largely involved in DNA repairs pathways, such as ATM and ATR, in the aetiology of the autism spectrum disorders and epilepsy. Both these pathological states are characterized by neuronal hyperexcitability and excitatory/inhibitory unbalance, thus in lab we are developing new pharmacological approaches on ATM and ATR, in order to normalize these neuronal defects and rescue brain functions. Finally, the role of ATM and ATR is being investigated in the laboratory also in the phenomena of aging and neurodegeneration of the hippocampal region.
5) Elena Chiricozzi https://www.unimi.it/it/ugov/person/elena-chiricozzi
Understanding the etiopathogenic mechanisms underlying the onset of Parkinson's disease. Two centuries after the disease was first described, to date no cure exists for Parkinson's disease patients. Particularly interesting is the role played by gangliosides, and specifically GM1 ganglioside, which negatively correlate with the disease and represent a new therapeutic frontier. This line of research is aimed at defining the etiopathogenetic mechanisms underlying the onset and progression of sporadic Parkinson's, highlighting the role of GM1 in relation to the cellular alterations described in the disease (mitochondrial dysfunction, excitotoxicity, inflammation, alpha-synuclein aggregation) and analyzing the affected areas (central nervous system, enteric, cardiac sympathetic) both in vitro and in vivo.
6) Raffaella Molteni https://www.unimi.it/it/ugov/person/raffaella-molteni
Role of the redox system and neuroinflammation in the vulnerability for psychiatric diseases. Psychiatric diseases are severe and highly diffuse disorders characterized by complex etiology and neurobiology. Despite the availability of several drugs, their use is associated with critical issues. Therefore, it is crucial to identify new pharmacological molecular targets in order to develop more efficient therapeutic strategies. Among the systems known to be altered in many of these diseases, redox balance and neuroinflammation play an important role. Accordingly, the aim of the project will be to investigate their involvement in the insurgence of these diseases and in the mechanism of action of the psychotropic drugs.
7) Francesco Bifari https://www.unimi.it/it/ugov/person/francesco-bifari
The project will study the therapeutic effect of a combined pharmacological approach to improve tissue regeneration and heal the hostile microenvironment present in conditions of impaired tissue regeneration. Such combined therapy will consist of the use of stem/precursor cells, the modulation of cell phenotypes through modification of cellular metabolism, the remodeling of the extracellular matrix, and the modulation of chronic inflammation. The proposed combined therapy will be tested on several degenerative conditions characterized by tissue loss, including neurodegenerative diseases. Careful investigation of the multiple molecular mechanisms of actions involving the therapeutic regenerative actions of the combined treatment will be performed. The impact of this regenerative approach will be evaluated by using several complementary catting edge techniques, and it will benefit from well renown national and international collaborations.
8) Maura Francolini https://www.unimi.it/it/ugov/person/maura-francolini
Accumulating evidence suggests that a broad spectrum of neurological defects is due to mutations in genes coding for synaptic proteins controlling synapse formation and maintenance, neuronal excitability and neurotransmission, neurotransmitter release and receptors signaling and trafficking. Similarly, mutations can affect genes associated to structural synaptic plasticity causing early and late onset neurological disorders. In the past years we have investigated, in in vitro and in vivo model systems how mutations in a number of genes causing neurodevelopmental and neurodegenerative disorders influence the structure of individual synapses and the organization of the neuronal network by using advanced imaging technologies.