
- laura.torres.g@universidadeuropea.es
- Facultad de Ciencias Biomédicas y Deporte - Málaga
Profesor adjunto
Dra. Laura Torres García
- Biomédicas y Salud
Doctora en Neurociencia, es una profesional curiosa y motivada, apasionada por la ciencia, el estudio del cerebro y la divulgación del conocimiento. Inició su trayectoria en la Universidad de Málaga y posteriormente trabajó en Múnich (Alemania), investigando los efectos de la hipoxia en el cerebro. Más tarde, realizó su doctorado en Lund (Suecia), centrado en los mecanismos moleculares de enfermedades neurodegenerativas como el Parkinson y el Alzheimer. Su experiencia internacional le ha permitido desarrollarse científicamente y adquirir una sólida perspectiva intercultural.
Actualmente, orienta su carrera hacia la divulgación y la educación, diseñando programas innovadores que fomentan la curiosidad, el pensamiento crítico y el aprendizaje activo.
Formación académica
Máster Universitario en Profesorado de ESO, Bachillerato, FP y Enseñanza de Idiomas
- Universidad de Málaga
- 2025 - 2026
PhD en Neurociencia
- Lund University
- 2018 - 2022
Máster en Neurociencia y Ciencias del Comportamiento
- Universidad Pablo de Olavide
- 2016 - 2017
Graduada en Biología
- Universidad de Málaga
- 2010 - 2016
Experiencia profesional
Titulaciones
Publicaciones
Monitoring the interactions between alpha-synuclein and Tau in vitro and in vivo using bimolecular fluorescence complementation
Parkinson’s and Alzheimer’s diseases involve aggregation of α-synuclein, Tau, and amyloid-β, often coexisting in mixed pathologies. This study used BiFC to test α-synuclein–Tau interaction in cell cultures and rodent models. Fluorescence signals confirmed their interaction in vitro and in vivo, particularly in the substantia nigra, demonstrating that these proteins interact in biologically relevant conditions and that BiFC is a useful tool to study these interactions.
Brain region-specific microglial and astrocytic activation in response to systemic lipopolysaccharides exposure
Microglia, the CNS immune cells, show strong regional heterogeneity in morphology, density, and inflammatory responses. This study examined their reaction across 16 brain regions after LPS-induced systemic inflammation, assessing morphological changes, sensitivity, and progression to chronic inflammation. Distinct region-specific responses were found, especially in the substantia nigra, with associated synaptic alterations. Partial CX3CR1 ablation reduced microglial activation and prevented chronic inflammation, highlighting it as a potential therapeutic target.
Astrocytic and Neuronal Apolipoprotein E Isoforms Differentially Affect Neuronal Excitability
Synaptic dysfunction is an early feature of Alzheimer’s disease, with ApoE4 as a key genetic risk factor. This study shows ApoE localizes near synapses and modulates neuronal activity depending on its source. Astrocyte-derived ApoE4 increases activity acutely, while neuron-derived ApoE3 drives higher firing rates. Effects differ in AD models, highlighting source- and isoform-specific roles of ApoE in neuronal excitability.