Cellular Neurophysiology


Group leader

Fabio Grohovaz


The work of Cellular neurophysiology Unit is aimed at understanding the molecular and cellular mechanisms underlying neuroprotection, neuroinflammation and neurodegeneration. Final objective is the identification of biomarkers and pharmacological targets for the prevention and cure of neurodegenerative diseases.

The brain is particularly vulnerable to toxic effects of reactive oxygen species and a clear correlation with neurodegeneration has been observed. This group is interested in the way oxidative stress is generated and protection mechanisms are activated in both neurons and astrocytes. In light of the relevance of neuroinflammatory processes in neurodegeneration, group interest is also focused on the molecular mechanisms involved in the process of glia activation and on the influence the activated phenotype has on neuronal survival.

It is well known that an increase in synaptic activity is potentially harmful for neurons, determining dysregulation of the ionic homeostasis as well as alterations of protein expression. In this respect, iron is an essential element required for many physiological functions, but it is also a key player in oxidative stress induction. Of note, iron accumulation within neurons is a condition that occurs physiologically with age but is also favoured in many neurodegenerative diseases.

Research activity

A research line of this lab is aimed at characterizing the physiological mechanisms of iron handling, at both cellular and mitochondrial level, in primary neurons and glial cells. Moreover, Induced Pluripotent Stem Cells (iPSCs) are employed in investigating the molecular mechanisms underlying Friedreich’s ataxia, as well as other neurodegenerative disorders characterized by alteration of intracellular iron homeostasis.

In another research line, this group investigates the effect of increased synaptic activity on the control of BACE1, the beta-secretase that triggers the amyloidogenic processing of the amyloid precursor protein thereby favouring deposition of the neurotoxic amyloid-beta peptide in the brain of Alzheimer’s disease patients. It has been provided evidence that BACE-1 expression is tightly regulated and that, even in the absence of an increase in the transcript, its expression can be controlled by translational regulation. The Unit is currently characterizing an initiation factor that is preferentially localized at synaptic microdomains and that is able to regulate the translation initiation of BACE1 in response to increased synaptic activity.