Person:
Leza Cerro, Juan Carlos

First Name

Juan Carlos

Last Name

Leza Cerro

Affiliation

Universidad Complutense de Madrid

Faculty / Institute

Medicina

Department

Farmacología y Toxicología

Area

Farmacología

Identifiers

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Search Results

Now showing 1 - 10 of 10

Study of Microbiota in MDD
(2020) Caso Fernández, Javier Rubén; Leza Cerro, Juan Carlos; MacDowell Mata, Karina Soledad
Raw Data: Sample ID, Relative abundances and Genera Reads
Elaboración de casos clínicos para el aprendizaje basado en casos prácticos: una herramienta pedagógica para la inmersión en la materia de profesores noveles y un recurso didáctico en la metodología de aprendizaje con participación del estudiante
(2023-07) Gutiérrez López, María Dolores; Caballero Collado, Ricardo; Caso, Javier; Delpón Mosquera, María Eva; García Bueno, Borja; Leza Cerro, Juan Carlos; Lizasoain, Ignacio; McDowell Mata, Karina; Morales, Daniel; Moreno Gutiérrez, Laura; Muñoz Madrigal, Jose Luis; O’Shea Gaya, María Esther; Pérez Vizcaíno, Francisco; Tejerina Maria, Teresa; Vidal Casado, Rebeca; Vidal, Alfonso; Martín Hernández, David; Malan-Müller, Stefanie; Olivencia, Miguel Ángel; Morales, Nuria; Núñez de la Calle, Carlos; Vicente Crespo, Maria Elena; Cogolludo Torralba, Ángel Luis
El proyecto propone la elaboración de nuevos casos clínicos que asemejen situaciones reales sobre los que los estudiantes puedan desarrollar un aprendizaje autónomo dirigido por el profesorado en función de los conceptos que sean de interés para cada grupo farmacológico y acercándole a la situación más cercana a su práctica profesional. Los objetivos del proyecto son: 1) Generar una base de nuevos casos clínicos dirigidos a que los estudiantes trabajen sobre grupos de fármacos en un contexto lo más real posible. Los diferentes casos que se elaboren en este proyecto podrán ser utilizados en la docencia de diversas asignaturas impartidas por miembros del departamento de Farmacología y Toxicología. Las sesiones dirigidas al estudio basado en la resolución de casos se plantean como una herramienta docente que tiene como finalidad el desarrollo de competencias transversales como promover la motivación, el trabajo en equipo, la participación de los estudiantes en los debates, así como, fomentar el pensamiento crítico y el conocimiento del método científico. Este tipo de aprendizaje en contexto facilita la integración de los conocimientos y su mayor retención además de la dotar a los estudiantes con las habilidades para fomentar un aprendizaje continuo. 2) Apoyar la formación del profesorado de reciente incorporación, así como del personal investigador que participan como colabores en tareas docentes del departamento y que podrían ser potenciales futuros docentes.
Neuroplasticity and inflammatory alterations in the nucleus accumbens are corrected after risperidone treatment in a schizophrenia-related developmental model in rats
(Elsevier, 2021-07-20) 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.
CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes
(MPDI, 2022-03-18) Gutiérrez Cañas, 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.
Gestión de exámenes online. Base de datos de preguntas y desarrollo de software
(2021-06-28) Pérez Vizcaíno, Francisco; Esquivel Ruiz, Sergio Antonio; Gil De Biedma Elduayen, Leticia; Macías Montero, Miguel; Morales Puerto, Nuria; Núñez De La Calle, Carlos; Olivencia Plaza, Miguel Ángel; Bas Caro, Manuel; Caso Fernandez, Javier Rubén; Cogolludo Torralba, Ángel Luis; García Bueno, Borja; Gutiérrez Lopez, María Dolores; Hurtado Moreno, Olivia; Leza Cerro, Juan Carlos; Moreno Gutiérrez, Laura; O'Shea Gaya, María Esther; Pradillo Justo, Jesús Miguel; Vidal Casado, Rebeca
Microglial CX3CR1 production increases in Alzheimer's disease and is regulated by noradrenaline
(Wiley, 2021-01) Muñoz Madrigal, José Luis; González Prieto, Marta; López Gutiérrez, Irene; García Bueno, Borja; Caso Fernández, Javier Rubén; Leza Cerro, Juan Carlos; Ortega Hernández, Adriana; Gómez Garre, Dulcenombre
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.
Noradrenaline in Alzheimer's Disease: A New Potential Therapeutic Target
(MDPI, 2022-05-30) 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.
Reboxetine Treatment Reduces Neuroinflammation and Neurodegeneration in the 5xFAD Mouse Model of Alzheimer's Disease: Role of CCL2
(Springer, 2019-07-11) López Gutiérrez, Irene; García Bueno, Borja; Caso Fernández, Javier Rubén; García Bueno, Borja; Leza Cerro, Juan Carlos; Muñoz Madrigal, José Luis
The reduction of brain noradrenaline levels is associated to the initiation of Alzheimer’s disease and contributes to its progression. This seems to be due mainly to the anti-neuroinflammatory actions of noradrenaline. The analysis of noradrenaline effects on brain cells demonstrates that it also regulates the production of the chemokine CCL2. In the present study, we analyzed the effect of the selective noradrenaline reuptake inhibitor, reboxetine, on the inflammatory and neurodegenerative alterations present in 5xFAD mice, and how the genetic removal of CCL2 affects reboxetine actions. We observed that the removal of CCL2 reduced the memory impairments in 5xFAD mice as well as the neuroinflammatory response, the accumulation of amyloid beta plaques, and the degeneration of neurons in the brain cortex. The administration of reboxetine with osmotic pumps for 28 days also resulted in anti-inflammatory and neuroprotective changes in 5xFAD mice, even in the absence of CCL2. Yet, 6-month-old CCL2KO mice presented a significant degree of neuroinflammation and neuronal damage. These findings indicate that reboxetine treatment prevents the brain alterations caused by prolonged overproduction of amyloid beta, being these effects independent of CCL2, which is a mediator of the damage caused by amyloid beta in the brain cortex, but necessary for the prevention of the development of neurodegeneration in normal healthy conditions.
Base de datos de preguntas y actualización del software. Herramientas para la generación de exámenes presenciales u online
(2022-09-30) O'Shea Gaya, María Esther; Pérez Vizcaíno, Francisco; Caso Fernández, Javier Rubén; Cogolludo Torralba, Ángel Luis; García Bueno, Borja; Gutiérrez López, María Dolores; Hurtado Moreno, Olivia; Leza Cerro, Juan Carlos; Moreno Gutiérrez, Laura; Pradillo Justo, Jesús Miguel; Vidal Casado, Rebeca; Esquivel Ruiz, Sergio Antonio; Gil De Biedma Elduayen, Leticia; Macías Montero, Miguel; Morales Puerto, Nuria; Núñez De La Calle, Carlos; Olivencia Plaza, Miguel Ángel; Bas Caro, Manuel; Morales Cano, Daniel
Noradrenaline in Alzheimer’s Disease: A New Potential Therapeutic Target
(MDPI, 2022-05-30) Gutiérrez Cañas, Irene; Dello Russo, Cinzia; 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.