We study the molecular basis of neurodegeneration and the role of glial cells in neurological diseases.
We study the molecular mechanisms underlying myelin degeneration and white matter loss in Alzheimer's disease. In particular, by using a combination of in vitro and in vivo models, as well as post-mortem human samples, we investigate how amyloid-beta signaling induce temporal and spatial control of locally translated protein in oligodendrocytes, affecting both cell physiology and morphology.
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.
We study the interaction between the extracellular matrix, the dynamic scaffold and signalling hub surrounding every cell, and microglia, the never-resting immune patrol of the brain. We explore this interplay in models of aging and brain pathology, coupled to fluorescence microscopy techniques and in vivo, ex vivo or 3D-in vitro paradigms, where we can modify the matrix and/or neuroinflammation experimentally.
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.