Browsing by Author "Soto, Paulina"

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    Manual para familiares (o cuidadores) de personas con Trastorno de Personalidad
    Fischer Perlman, Candice; Soto, Paulina; Errázuriz Arellano, Paula
    Manual Psicoeducativo que tiene como objetivo dar información a aquellas personas que cuidan y/o acompañan a algún ser querido con trastorno de personalidad. Este trabajo se enmarca dentro de una colaboración entre la Escuela de Psicología UC y la fundación PsiConecta, con el apoyo de MIDAP.
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    The necroptosis machinery mediates axonal degeneration in a model of Parkinson disease
    (2020) Onate, Maritza; Catenaccio, Alejandra; Salvadores, Natalia; Saquel, Cristian; Martinez, Alexis; Moreno-Gonzalez, Ines; Gamez, Nazaret; Soto, Paulina; Soto, Claudio; Hetz, Claudio; Court, Felipe A.
    Parkinson's disease (PD) is the second most common neurodegenerative condition, characterized by motor impairment due to the progressive degeneration of dopaminergic neurons in the substantia nigra and depletion of dopamine release in the striatum. Accumulating evidence suggest that degeneration of axons is an early event in the disease, involving destruction programs that are independent of the survival of the cell soma. Necroptosis, a programmed cell death process, is emerging as a mediator of neuronal loss in models of neurodegenerative diseases. Here, we demonstrate activation of necroptosis in postmortem brain tissue from PD patients and in a toxin-based mouse model of the disease. Inhibition of key components of the necroptotic pathway resulted in a significant delay of 6-hydroxydopamine-dependent axonal degeneration of dopaminergic and cortical neurons in vitro. Genetic ablation of necroptosis mediators MLKL and RIPK3, as well as pharmacological inhibition of RIPK1 in preclinical models of PD, decreased dopaminergic neuron degeneration, improving motor performance. Together, these findings suggest that axonal degeneration in PD is mediated by the necroptosis machinery, a process here referred to as necroaxoptosis, a druggable pathway to target dopaminergic neuronal loss.