Molecular Neuroembriology Lab

The Laboratory of Molecular Neuroembriology conducts research on macro-autophagy, an intracellular degradation mechanism that plays a central role in the physical-chemical equilibrium tissue maintenance (homeostasis). The research yielded the identification of a new protein (AMBRA1), which acts as an activator of autophagy and participates in the development of the nervous system. The Laboratory has also highlighted the role of AMBRA1 in the process of proliferation of tumor cells, demonstrating that in conditions of stress or lack of nutrients the protein regulates the levels of c-myc, the oncogene to the base of cell multiplication. If not under control, c-myc increases in an irregular manner the proliferation mechanism and causes the onset of tumors. The research team is evaluating the role played by the different diet regimes (Mediterranean, rich, high protein) in autophagy regulation and tumorigenesis.

Mechanism of Differentiation of T-Lymphocytes

The research activity of the Laboratory also relates to the mechanisms underlying the differentiation of T-cells, which exert a suppressive function on the population of effector T-lymphocytes, preventing them from triggering autoimmune responses. The balance guaranteed by cell homeostasis plays a central role in protecting the body and the presence of autoreactive T-lymphocytes, which can attack the body components, is controlled by peripheral tolerance. When the peripheral tolerance mechanism stops working, the development of autoreactive T-cells can give rise to autoimmune diseases such as multiple sclerosis.

Alzheimer's Disease

A further scope of the Laboratory research concerns the pathogenesis of Alzheimer's disease and the role played by autophagy in dendritic spines, the protrusions or dendrites of the neuron that isolate and amplify electrical signals received at synapses. The laboratory has shown that early degeneration of dendritic spines, that the basis of Alzheimer's disease, is related to mitochondrial anomalies. It remains unclear, and is currently being studied, what the role of morphological abnormalities of mitochondria is in the formation of the disease and the importance of autophagy in the process of elimination of damaged mitochondria. The objective is to develop molecules capable of regulating autophagy and establishing a therapeutic strategy against neurodegeneration, devoid of the side effects typically induced by drug treatment.