We are interested in understanding how mitochondrial metabolism regulates neuronal responses in disease models.
In our increasingly ageing society, neurodegenerative diseases are posing a major burden. A growing body of evidence has linked alterations in metabolism and mitochondrial function to some of the most devastating forms of neurodegeneration, including Parkinson´s disease, cerebellar ataxias and peripheral neuropathies. However, despite the urge to find strategies to prevent or arrest neurodegeneration, our understanding of the precise events underlying neuronal death caused by mitochondrial dysfunction is very limited.
We recently identified the activation of metabolic stress responses in dysfunctional neurons, which we showed to be essential in sustaining neuronal viability when mitochondrial function is compromised. These findings suggest a previously unappreciated degree of metabolic flexibility in nerve cells that provide new mechanistic insights into the processes leading to neurodegeneration.
Building on these premises, our lab is currently working on understanding the regulatory checkpoints behind this metabolic rewiring with the aim manipulate them for reverting degeneration.
Unraveling the mechanisms behind metabolic rewiring in dysfunctional neurons holds promise for developing therapeutic approaches that could potentially slow or halt the progression of neurodegenerative disorders.