Person:
Muñoz Madrigal, José Luis

First Name

José Luis

Last Name

Muñoz Madrigal

URI

https://hdl.handle.net/20.500.14352/79063

Affiliation

Universidad Complutense de Madrid

Faculty / Institute

Medicina

Department

Farmacología y Toxicología

Area

Farmacología

Identifiers

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Now showing 1 - 8 of 8

Project number: 102
Empleo de la gamificación como nueva herramienta docente en la asignatura de Intervención en adicciones dentro del grado de Terapia Ocupacional
(2020) Muñoz Madrigal, José Luis; García Bueno, Borja; Caso Fernández, Javier Rubén; López Gutiérrez, Irene; González Prieto, Marta; Bas Caro, Manuel
El principal objetivo de este proyecto ha sido el de mejorar los resultados académicos de los alumnos así como aumentar su interés por la asignatura, su asistencia y participación en clase. Además, se pretendía obtener datos que demuestren la utilidad de la gamificación como herramienta docente en nuestro ámbito y animar a otros profesores a realizar innovaciones similares.
Neuroplasticity and inflammatory alterations in the nucleus accumbens are corrected after risperidone treatment in a schizophrenia-related developmental model in rats
(Schizophrenia Research, 2021) Tendilla Beltrán, Hiram; Coatl Cuaya, Heriberto; Meneses Prado, Silvia; Vázquez Roque, Ruben Antonio; Brambila, Eduardo; Tapia Rodríguez, Miguel; Martín Hernández, David; Garcés Ramírez, Linda; Muñoz Madrigal, José Luis; Leza Cerro, Juan Carlos; Flores, Gonzalo
Increased dopaminergic activity in the striatum underlies the neurobiology of psychotic symptoms in schizophrenia (SZ). Beyond the impaired connectivity among the limbic system, the excess of dopamine could lead to inflammation and oxidative/nitrosative stress. It has been suggested that atypical antipsychotic drugs attenuate psychosis not only due to their modulatory activity on the dopaminergic/serotonergic neurotransmission but also due to their anti-inflammatory/antioxidant effects. In such a manner, we assessed the effects of the atypical antipsychotic risperidone (RISP) on the structural neuroplasticity and biochemistry of the striatum in adult rats with neonatal ventral hippocampus lesion (NVHL), which is a developmental SZ-related model. RISP administration (0.25 mg/kg, i.p.) ameliorated the neuronal atrophy and the impairments in the morphology of the dendritic spines in the spiny projection neurons (SPNs) of the ventral striatum (nucleus accumbens: NAcc) in the NVHL rats. Also, RISP treatment normalized the pro-inflammatory pathways and induced the antioxidant activity of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in this model. Our results point to the neurotrophic, antiinflammatory, and antioxidant effects of RISP, together with its canonical antipsychotic mechanism, to enhance striatum function in animals with NVHL.
Noradrenaline in Alzheimer's Disease: A New Potential Therapeutic Target
(2022) Muñoz Madrigal, José Luis; López Gutiérrez, Irene; Dello Russo, Cinzia; Novellino, Fabiana; Caso Fernández, Javier Rubén; García Bueno, Borja; Leza Cerro, Juan Carlos
A growing body of evidence demonstrates the important role of the noradrenergic system in the pathogenesis of many neurodegenerative processes, especially Alzheimer’s disease, due to its ability to control glial activation and chemokine production resulting in anti-inflammatory and neuroprotective effects. Noradrenaline involvement in this disease was first proposed after finding deficits of noradrenergic neurons in the locus coeruleus from Alzheimer’s disease patients. Based on this, it has been hypothesized that the early loss of noradrenergic projections and the subsequent reduction of noradrenaline brain levels contribute to cognitive dysfunctions and the progression of neurodegeneration. Several studies have focused on analyzing the role of noradrenaline in the development and progression of Alzheimer’s disease. In this review we summarize some of the most relevant data describing the alterations of the noradrenergic system normally occurring in Alzheimer’s disease as well as experimental studies in which noradrenaline concentration was modified in order to further analyze how these alterations affect the behavior and viability of different nervous cells. The combination of the different studies here presented suggests that the maintenance of adequate noradrenaline levels in the central nervous system constitutes a key factor of the endogenous defense systems that help prevent or delay the development of Alzheimer’s disease. For this reason, the use of noradrenaline modulating drugs is proposed as an interesting alternative therapeutic option for Alzheimer’s disease.
Project number: 194
Universidad inclusiva para la promoción de una sociedad inclusiva.
(2022) Pérez Martínez, Sara; Funes Lapponi, Silvina Graciela; García Momblán, María Cristina; Gaya Barroso, Aina; Muñoz Madrigal, José Luis; Pavón Mestras, Juan Luis; Trujillo Barbadillo, Gracia
Nuestro proyecto pretende desarrollar recursos y estrategias innovadoras para la promoción de la inclusión de la diversidad en la comunidad universitaria orientados a la mejora social de los colectivos vulnerables en colaboración con otros agentes sociales.
Microglial CX3CR1 production increases in Alzheimer's disease and is regulated by noradrenaline
(Glia, 2021) González Prieto, Marta; López Gutiérrez, Irene; García Bueno, Borja; Caso Fernández, Javier Rubén; Leza Cerro, Juan Carlos; Ortega Hernández, Adriana; Gómez Garre, María Dulce Nombre; Muñoz Madrigal, José Luis
The loss of noradrenergic neurons and subsequent reduction of brain noradrenaline (NA) levels are associated with the progression of Alzheimer's disease (AD). This seems to be due mainly to the ability of NA to reduce the activation of microglial cells. We previously observed that NA induces the production of the chemokine Fractalkine/CX3CL1 in neurons. The activation of microglial CX3CR1, sole receptor for CX3CL1, reduces the activation of microglia, which is known to largely contribute to the neuronal damage characteristic of AD. Therefore, alterations of CX3CR1 production in microglia could translate into the enhancement or inhibition of CX3CL1 anti-inflammatory effects. In order to determine if microglial CX3CR1 production is altered in AD and if NA can control it, CX3CR1 expression and synthesis were analyzed in 5xFAD mice and human AD brain samples. In addition, the effects of NA and its reuptake inhibitor reboxetine were analyzed in microglial cultures and mice respectively. Our results indicate that in AD CX3CR1 production is increased in the brain cortex and that reboxetine administration further increases it and enhances microglial reactivity toward amyloid beta plaques. However, direct administration of NA to primary rat microglia or human HMC3 cells inhibits CX3CR1 production, suggesting that microglia responses to NA may be altered in the absence of CX3CL1-producing neurons or other nonmicroglial external factors.
CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes
(International Journal of Molecular Sciences, 2022) López Gutiérrez, Irene; Novellino, Fabiana; Caso Fernández, Javier Rubén; García Bueno, Borja; Leza Cerro, Juan Carlos; Muñoz Madrigal, José Luis
The chemokine CCL2 participates in multiple neuroinflammatory processes, mainly through the recruitment of glial cells. However, CCL2 has also been proven to exert different types of actions on these cells, including the modification of their response to inflammatory stimuli. In the present study we analyzed the effect of CCL2 on the resolution of inflammation in astrocytes. We observed that genetic removal of CCL2 increases the expression of the enzymes responsible for the synthesis of specialized pro-resolving mediators arachidonate 15-lipoxygenase and arachidonate 5-lipoxygenase in the brain cortex of 5xFAD mice. The expression of FPR2 receptor, known to mediate the activity of pro-resolving mediators was also increased in mice lacking CCL2.The downregulation of these proteins by CCL2 was also observed in cultured astrocytes. This suggests that CCL2 inhibition of the resolution of inflammation could facilitate the progression of neuroinflammatory processes. The production of the pro-inflammatory cytokine IL-1beta by astrocytes was analyzed, and allowed us to confirm that CCL2 potentiates the activation of astrocytes trough the inhibition of pro-resolving pathways mediated by Resolvin D1. In addition, the analysis of the expression of TNFalpha, MIP1alpha and NOS2 further confirmed CCL2 inhibition of inflammation resolution in astrocytes.
Intervención en adicciones: hacia una intervención centrada en la persona desde el Aprendizaje-Servicio
(2020) Muñoz Madrigal, José Luis; Pérez Martínez, Sara; Rubio Valladolid, Gabriel; Arias Horcajadas, Francisco
Noradrenaline in Alzheimer’s Disease: A New Potential Therapeutic Target
(International Journal of Molecular Sciences, 2022) López Gutiérrez, Irene; Novellino, Fabiana; Caso Fernández, Javier Rubén; García Bueno, Borja; Leza Cerro, Juan Carlos; Muñoz Madrigal, José Luis
A growing body of evidence demonstrates the important role of the noradrenergic system in the pathogenesis of many neurodegenerative processes, especially Alzheimer’s disease, due to its ability to control glial activation and chemokine production resulting in anti-inflammatory and neuroprotective effects. Noradrenaline involvement in this disease was first proposed after finding deficits of noradrenergic neurons in the locus coeruleus from Alzheimer’s disease patients. Based on this, it has been hypothesized that the early loss of noradrenergic projections and the subsequent reduction of noradrenaline brain levels contribute to cognitive dysfunctions and the progression of neurodegeneration. Several studies have focused on analyzing the role of noradrenaline in the development and progression of Alzheimer’s disease. In this review we summarize some of the most relevant data describing the alterations of the noradrenergic system normally occurring in Alzheimer’s disease as well as experimental studies in which noradrenaline concentration was modified in order to further analyze how these alterations affect the behavior and viability of different nervous cells. The combination of the different studies here presented suggests that the maintenance of adequate noradrenaline levels in the central nervous system constitutes a key factor of the endogenous defense systems that help prevent or delay the development of Alzheimer’s disease. For this reason, the use of noradrenaline modulating drugs is proposed as an interesting alternative therapeutic option for Alzheimer’s disease.