Person:
Ramos Atance, José Antonio

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First Name
José Antonio
Last Name
Ramos Atance
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Odontología
Department
Bioquímica y Biología Molecular
Area
Bioquímica y Biología Molecular
Identifiers
UCM identifierORCIDScopus Author IDDialnet ID

Search Results

Now showing 1 - 9 of 9
  • Publication
    Puesta en marcha del curso on line “Envejecimiento y enfermedades neurodegenerativas” en la plataforma Miriadax
    (2019-03-30) Lago Femia, Eva de; Sagredo Ezquioga, Onintza; García Garcia, María Concepción; Hernández Galvez, María Luz; Gómez Ruiz, María; Ramos Atance, José Antonio; Fernandez Ruiz, José Javier; Rodríguez Cueto, Carmen; de Castro Vitores, Jacinto; López Blanco, Olga; Esteban Cubero, Amparo; Satta, Valentina; Espejo Porras, Francisco; Santos-García, Irene; García Toscano, Laura; Alonso Gómez, Cristina
    Este informe detalla los objetivos, actividades y métodos llevados a cabo durante la ejecución de un proyecto de innovación docente que tiene como objetivo implementar un curso online en abierto sobre las enfermedades neurodegenerativas y el envejecimiento.
  • Publication
    Experiencia sobre la evaluación continua a través de Campus Virtual
    (Universidad Complutense de Madrid, 2012) Lago Femia, Eva de; Sagredo Ezkioga, Onintza; Ramos Atance, José Antonio
    Los métodos digitales están adquiriendo cada vez más importancia dentro del proceso de aprendizaje por las ventajas que aportan y por la demanda de los alumnos. Sin embargo, uno de los retos más complicados que se nos plantean con los nuevos planes docentes es llegar a conseguir un método efectivo de evaluación continua sobre el trabajo de los alumnos. Es por lo tanto, importante el realizar experiencias encaminadas a desarrollar diferentes estrategias que lo permitan, aprovechando las herramientas que aportan las nuevas plataformas digitales.
  • Publication
    Estructura y función del complejo multienzimático ácido graso sintetasa de ceratitis capitata
    (Universidad Complutense de Madrid, 2015) Ramos Atance, José Antonio; Martín Municio, Ángel
  • Publication
    Actas: Reunión Iberoamericana sobre cannabis medicinal
    (Carlos Brito Siso, 2020-11) Ramos Atance, José Antonio; Guzmán Pastor, Manuel; Manjón-Cabeza Olmeda, Araceli; Brito Siso, Carlos; Vitale Marino, Augusto; Reyes Alvarado, Yesid; Snapp, Zara; Pérez Martínez, Jordi; Pineda-Villegas, Paola; Peyraube, Raquel
    El día 5 de marzo de 2020 –a una semana de entrar en estado de alarma, con confinamientos, restricciones y vuelta al estado de alarma- pudimos celebrar en la Facultad de Ciencias de la Información de la Universidad Complutense de Madrid una reunión sobre cannabis medicinal. La organización se enmarca en una línea estrecha línea de colaboración mantenida durante los últimos años entre el Instituto Universitario de Investigación en Neuroquímica y el Proyecto de Investigación “Fiscalización internacional de drogas: problemas y soluciones”. Una vez más, quienes desde la UCM estudiamos distintos aspectos del cannabis medicinal, quisimos poner de manifiesto tres cuestiones. La primera, que a día de hoy existen evidencias suficientes sobre la utilidad medicinal del cannabis. La segunda, que resulta sin duda deseable obtener más evidencias, lo que requiere más investigación. Y, la tercera, que es necesario un marco legal que permita esa investigación y la dispensación del cannabis medicinal, como ocurre ya en muchos países de todo el planeta. En la reunión contamos con expertos de distintas áreas y del máximo nivel en sus respectivos ámbitos de salud o políticas legislativas. Sus valiosas aportaciones se recogen ahora y se hacen públicas como documentos muy relevantes en una discusión que continúa viva y que debemos seguir alimentando para que el conocimiento científico y la necesidad de los pacientes dejen de enfrentarse a unas políticas legislativas, nacionales e internacionales, irracionales y que desprecian dos enfoques básicos: el enfoque científico y el enfoque de derechos humanos. Especialmente relevante es la reciente posición de la OMS sobre el cannabis medicinal. En 2017 este organismo decidió realizar una revisión crítica sobre el valor medicinal de la planta, sus principios activos y algunos imitadores de síntesis. Las razones que llevaron a esta revisión fueron explicitadas así por la OMS: 1ª) No hay evidencias de muertes por sobredosis. 2ª) Es una sustancia relativamente segura. 3ª) Existe abundante literatura preclínica que avala su efectividad en cáncer, dolor crónico, dolor neuropático, epilepsias pediátricas, estimulación de apetito, estrés postraumático, trastornos del sueño y dependencia a opiáceos. 4ª) Los efectos adversos son posibles, pero leves. 5ª) La clasificación actual del cannabis como droga muy peligrosa, muy adictiva y sin ninguna indicación terapéutica no se justifica. Tras analizar evidencias y bibliografía, la OMS propuso a la Comisión de Estupefacientes una reclasificación del cannabis que permitiese su uso medicinal y facilitase la investigación sobre el potencial médico; además se indicaba que los extractos y las tinturas y el principio activo CBD no deberían ser objeto de clasificación en las Convenciones de drogas. La Comisión de Estupefacientes, sin razón que lo justifique, ha pospuesto por dos veces, en 2019 y en 2020, pronunciarse sobre las recomendaciones de la OMS. Se espera para diciembre de 2020 otra reunión de la Comisión de Estupefacientes en la que debería pronunciarse aceptando las recomendaciones, evitando así que dentro de Naciones Unidas existan dos voces opuestas sobre una misma cuestión. Con todo, son muchos los países y territorios que, sin esperar a la reclasificación en Naciones Unidas, han reglamentado programas de dispensación de cannabis medicinal. Se trata en concreto de Italia, Reino Unido, Portugal, Holanda, Alemania, República Checa, Dinamarca, Luxemburgo, Finlandia, Polonia, Israel, Canadá, Uruguay, Colombia, Perú, Chile, Argentina, Costa Rica, Ecuador, Jamaica, Sudáfrica, Malaui, Zimbabue, Tailandia, Australia, Nueva Zelanda y 33 estados de EE. UU. España posee condiciones y modelos suficientes para acometer prontamente la regulación del cannabis medicinal; solo falta la voluntad política de hacerlo.
  • Publication
    Aumentando la presencia de la UCM en los MOOCs: Puesta en marcha de un curso online sobre neurociencia
    (2017-06-30) De Lago Femia, Eva; Ramos Atance, José Antonio; Fernández Ruiz, José Javier; Sagredo Esquioga, Onintza; García García, María Concepción; Rodríguez Cueto, Carmen
  • Publication
    Altered striatal endocannabinoid signaling in a transgenic mouse model of spinocerebellar ataxia type-3
    (PLOS, 2017-04-27) Hernández-Gálvez, Mariluz; Hillard, Cecilia J.; Maciel, Patricia; Valdeolivas, Sara; Rodríguez Cueto, Carmen Aurora; Gómez Ruiz, María Sagrario; Fernández Ruiz, José Javier; Ramos Atance, José Antonio; David R Borchelt
    Spinocerebellar ataxia type-3 (SCA-3) is the most prevalent autosomal dominant inherited ataxia. We recently found that the endocannabinoid system is altered in the post-mortem cerebellum of SCA-3 patients, and similar results were also found in the cerebellar and brainstem nuclei of a SCA-3 transgenic mouse model. Given that the neuropathology of SCA-3 is not restricted to these two brain regions but rather, it is also evident in other structures (e.g., the basal ganglia), we studied the possible changes to endocannabinoid signaling in the striatum of these transgenic mice. SCA-3 mutant mice suffer defects in motor coordination, balance and they have an abnormal gait, reflecting a cerebellar/brainstem neuropathology. However, they also show dystonia-like behavior (limb clasping) that may be related to the malfunction/deterioration of specific neurons in the striatum. Indeed, we found a loss of striatal projecting neurons in SCA-3 mutant mice, accompanied by a reduction in glial glutamate transporters that could potentially aggravate excitotoxic damage. In terms of endocannabinoid signaling, no changes in CB2 receptors were evident, yet an important reduction in CB1 receptors was detected by qPCR and immunostaining. The reduction in CB1 receptors was presumed to occur in striatal afferent and efferent neurons, also potentially aggravating excitotoxicity. We also measured the endocannabinoid lipids in the striatum and despite a marked increase in the FAAH enzyme in this area, no overall changes in these lipids were found. Collectively, these studies confirm that the striatal endocannabinoid system is altered in SCA-3 mutant mice, adding to the equivalent changes found in other strongly affected CNS structures in this type of ataxia (i.e.: the cerebellum and brainstem). These data open the way to search for drugs that might correct these changes.
  • Publication
    Dysregulation of the endocannabinoid signaling system in the cerebellum and brainstem in a transgenic mouse model of spinocerebellar ataxia type-3
    (Elsevier, 2016-12) Hernández-Gálvez, Mariluz; Hillard, Cecilia J.; Maciel, Patricia; García-García, Luis; Valdeolivas, Sara; Rodríguez Cueto, Carmen Aurora; Pozo García, Miguel Ángel; Ramos Atance, José Antonio; Gómez Ruiz, María Sagrario; Fernández Ruiz, José Javier; García García, Luis
    Spinocerebellar ataxia type-3 (SCA-3) is a rare disease but it is the most frequent type within the autosomal dominant inherited ataxias. The disease lacks an effective treatment to alleviate major symptoms and to modify disease progression. Our recent findings that endocannabinoid receptors and enzymes are significantly altered in the post-mortem cerebellum of patients affected by autosomal-dominant hereditary ataxias suggest that targeting the endocannabinoid signaling system may be a promising therapeutic option. Our goal was to investigate the status of the endocannabinoid signaling system in a transgenic mouse model of SCA-3, in the two CNS structures most affected in this disease - cerebellum and brainstem. These animals exhibited progressive motor incoordination, imbalance, abnormal gait, muscle weakness, and dystonia, in parallel to reduced in vivo brain glucose metabolism, deterioration of specific neuron subsets located in the dentate nucleus and pontine nuclei, small changes in microglial morphology, and reduction in glial glutamate transporters. Concerning the endocannabinoid signaling, our data indicated no changes in CB2 receptors. By contrast, CB1 receptors increased in the Purkinje cell layer, in particular in terminals of basket cells, but they were reduced in the dentate nucleus. We also measured the levels of endocannabinoid lipids and found reductions in anandamide and oleoylethanolamide in the brainstem. These changes correlated with an increase in the FAAH enzyme in the brainstem, which also occurred in some cerebellar areas, whereas other endocannabinoid-related enzymes were not altered. Collectively, our results in SCA-3 mutant mice confirm a possible dysregulation in the endocannabinoid system in the most important brain structures affected in this type of ataxia, suggesting that a pharmacological manipulation addressed to correct these changes could be a promising option in SCA-3.
  • Publication
    Prospects for cannabinoid therapies in basal ganglia disorders
    (Wiley, 2011-07-12) Moreno‐Martet, Miguel; Palomo‐Garo, Cristina; Valdeolivas, Sara; Guaza, Carmen; Romero, Julián; Mechoulam, Raphael; Gómez Cañas, María; Fernández Ruiz, José Javier; Rodríguez Cueto, Carmen Aurora; Guzmán Pastor, Manuel; Ramos Atance, José Antonio
    Cannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannabinoids being effective in these disorders. On the one hand, cannabinoids like Δ9-tetrahydrocannabinol or cannabidiol protect nigral or striatal neurons in experimental models of both disorders, in which oxidative injury is a prominent cytotoxic mechanism. This effect could be exerted, at least in part, through mechanisms independent of CB1 and CB2 receptors and involving the control of endogenous antioxidant defences. On the other hand, the activation of CB2 receptors leads to a slower progression of neurodegeneration in both disorders. This effect would be exerted by limiting the toxicity of microglial cells for neurons and, in particular, by reducing the generation of proinflammatory factors. It is important to mention that CB2 receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up-regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB2 receptor up-regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB2 receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB2 receptors may represent promising therapeutic agents in HD and PD, thus deserving a prompt clinical evaluation.
  • Publication
    Prospects for cannabinoid therapies in basal ganglia disorders
    (Wiley Online Library, 2011-07-12) Moreno‐Martet, Miguel; Palomo‐Garo, Cristina; Valdeolivas, Sara; Guaza, Carmen; Romero, Julián; Mechoulam, Raphael; Fernández Ruiz, José Javier; Rodríguez Cueto, Carmen Aurora; Gómez Cañas, María; Guzmán Pastor, Manuel; Ramos Atance, José Antonio
    Cannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannabinoids being effective in these disorders. On the one hand, cannabinoids like Δ9‐tetrahydrocannabinol or cannabidiol protect nigral or striatal neurons in experimental models of both disorders, in which oxidative injury is a prominent cytotoxic mechanism. This effect could be exerted, at least in part, through mechanisms independent of CB1 and CB2 receptors and involving the control of endogenous antioxidant defences. On the other hand, the activation of CB2 receptors leads to a slower progression of neurodegeneration in both disorders. This effect would be exerted by limiting the toxicity of microglial cells for neurons and, in particular, by reducing the generation of proinflammatory factors. It is important to mention that CB2 receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up‐regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB2 receptor up‐regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB2 receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB2receptors may represent promising therapeutic agents in HD and PD, thus deserving a prompt clinical evaluation.