We study the molecular basis of neurodegeneration and the role of glial cells in neurological diseases.

We want to understand the role of astrocytes in the onset and development of Parkinson's disease (PD). Mounting evidence suggests that astrocytes may contribute to dopaminergic neurodegeneration through decreased homeostatic support and deficient neuroprotection. To clarify the role of astrocytes in PD, we use different human models: From induced pluripotent stem cells (iPSC)-derived astrocytes to the more complex midbrain organoids from PD patients.

Disruption of calcium homeostasis is a hallmark of most CNS diseases and therefore a research field of high therapeutic interest. Overactivation of glutamate receptors produces a cytosolic calcium overload that causes excitotoxic death of neurons and oligodendrocytes and contributes to acute and neurodegenerative disorders such as stroke and Alzheimer´s disease. We are focused on the role of both mitochondria and endoplasmic reticulum (ER), the most important Ca2+ stores inside the cell.

Myelin pathology is a feature of numerous neurodegenerative diseases. We study mechanisms of myelin de- and re-generation, with a particular interest in oligodendroglial energy homeostasis, and potential strategies to improve remyelination in the disease. 

Our research is focused on the role on neurotransmitter receptors in glial cells. We found that neurotransmitters can be deleterious to oligodendrocyte viability or promote maturation and myelination  Given the potential to modulate oligodendrocyte plasticity through the neurotransmitter GABA, we study the molecular mechanisms associated to GABAB receptor activation in the oligodendroglial lineage and the impact of GABAB receptor modulation in models of demyelination.