Saila: Neurozientziak

Ikastegia: Medikuntza eta Erizaintza Fakultatea

Campusa: Bizkaia

Ezagutza arloa: Osasun Zientziak

Eremua: Giza Anatomia eta Enbriologia

Ikerketa taldea: Neurobiologiako Laborategia

Talde hauen parte izan zen:

E-maila: carlos.matute@ehu.eus

Web-orri pertsonala: https://www.neurobiologylab.org/

Doctor/a por la Universidad de Zaragoza con la tesis Estudio experimental de la distribución de neurotransmisores en la vía córtico-celular y tacto-talémica 1982. Tesiaren zuzendaria Dr/a. Luis Martínez Millán.

1-Scientific contributions After returning to Spain in 1988, I founded the Laboratory of Neurobiology at the University of País Vasco. The focus of the lab was to study the cell biology of neurotransmitter receptors present in glia (astrocytes, oligodendrocytes and microglia) as well as their functional and pathological relevance. Among other findings, my laboratory discovered that oligodendrocytes and myelin are highly vulnerable to glutamate and purinergic agonists, a feature that is relevant to multiple sclerosis and brain ischemia. Importantly, we unveiled numerous potential therapeutic targets in these diseases, by characterizing the nature of the receptors involved in oligodendroglial toxicity and the signaling cascades they trigger. These findings have been published in high impact journals including PNAS, J Neurosci, Glia, TINS, and Cell Death Dis.; and uncovered the now extended and accepted view that glutamate and ATP excitoxicity of oligodendrocytes contributes to tissue damage in multiple sclerosis and neurodegenerative diseases. On the other hand, we recently found that activation of specific subtypes of purine receptors contributes to remyelination by promoting a regenerative phenotype of microglia; and that these cells are relevant to antigen presentation in multiple sclerosis (published in EMBO J Med and Cell Death Dis.). Moreover, we discovered that baclofen promotes remyelination of demyelinating lesions setting the preclinical ground for repurposing this GABAB agonist as a treatment for demyelinating disorders (published in Glia last year). In addition, my laboratory found molecular and cellular mechanisms occurring in neurons and glia that contribute to the pathophysiology of Alzheimer disease and Parkinson (PD). Thus, we observed that Aβ 1-42 oligomers kill neurons by activating NMDA receptors, damage astrocytes via β1 integrin signaling, and favor oligodendrocyte maturation that causes hypermyelination and axonal dysfunction (published in Cell Calcium, Aging Cell, Cell Death Dis., among others). Lastly, we found that pathogenic human -synuclein in Lewy bodies from PD brains propagates via the astroglia syncytium (published in Neurobiol. Dis. and Nat Comm). My group is a member of CIBERNED since 2007. This helped developing numerous national collaborations (12). In turn, my laboratory has a profound internalization reflected both in the attraction of funding (12 grants since 2012) and collaborative publications (around 50 in the last 10 years). Finally, my laboratory is truly multidisciplinary and the technical expertise of its members extends from microscopy (confocal, superresolution, 2-PM in vitro and in vivo, EM), immunochemistry, electrophysiology, to common and updated cell and molecular neurobiology techniques.