Person: Gómez Miguel, Begoña
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First Name
Begoña
Last Name
Gómez Miguel
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Biológicas
Department
Bioquímica y Biología Molecular
Area
Bioquímica y Biología Molecular
Identifiers
8 results
Search Results
Now showing 1 - 8 of 8
- PublicationSmall GSK-3 Inhibitor Shows Efficacy in a Motor Neuron Disease Murine Model Modulating Autophagy(Public Library of Sciences (PLOS), 2016-09-15) Munk, Estefanía de; Palomo, Valle; Muñoz Sáez, Emma; Pérez, Daniel I.; Gómez Miguel, Begoña; Solas Alados, Mª Teresa; Gil, Carmen; Martínez, Ana; Arahuetes Portero, Rosa MaríaAmyotrophic lateral sclerosis (ALS) is a progressive motor neuron degenerative disease that has no effective treatment up to date. Drug discovery tasks have been hampered due to the lack of knowledge in its molecular etiology together with the limited animal models for research. Recently, a motor neuron disease animal model has been developed using β-Nmethylamino-L-alanine (L-BMAA), a neurotoxic amino acid related to the appearing of ALS. In the present work, the neuroprotective role of VP2.51, a small heterocyclic GSK-3 inhibitor, is analysed in this novel murine model together with the analysis of autophagy. VP2.51 daily administration for two weeks, starting the first day after L-BMAA treatment, leads to total recovery of neurological symptoms and prevents the activation of autophagic processes in rats. These results show that the L-BMAA murine model can be used to test the efficacy of new drugs. In addition, the results confirm the therapeutic potential of GSK-3 inhibitors, and specially VP2.51, for the disease-modifying future treatment of motor neuron disorders like ALS.
- PublicationMorphometric and neurochemical alterations found in l-BMAA treated rats(Elsevier, 2015-05) Munck García, Estefanía de; Muñoz Sáez, Emma; Gómez Miguel, Begoña; Solas Alados, Mª Teresa; Martínez, Ana; Arahuetes, Rosa MaríaAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive muscle paralysis that reflects the motoneurons’ degeneration. Several studies support the relationship between β-N-methylamino-L-alanine (L-BMAA), a neurotoxic amino acid produced by cyanobacteria and diatoms, and the sporadic occurrence of ALS and other neurodegenerative diseases. Therefore, the study of its neurotoxicity mechanisms has assumed great relevance in recent years. Recently, our research team has proposed a sporadic ALS animal model by L-BMAA administration in rats, which displays many pathophysiological features of human ALS. In this paper, we deepen the characterization of this model corroborating the occurrence of alterations present in ALS patients such as decreased muscle volume, thinning of the motor cortex, enlarged brain's lateral ventricles, and alteration of both bulbar nuclei and neurotransmitters’ levels. Therefore, we conclude that L-BMAA treated rats could be a good model which mimics degenerative features that ALS causes in humans.
- PublicationNeuroprotective role of sphingosine-1-phosphate in L-BMAA treated neuroblastoma cells (SH-SY5Y)(Elsevier, 2015-04-23) Muñoz Sáez, Emma; Munck García, Estefanía de; Arahuetes Portero, Rosa María; Vicente, Francisca; Ortiz López, Francisco Javier; Cantizani, Juan; Gómez Miguel, BegoñaSphingosine-1-phosphate (S1P) is a bioactive lipid which regulates proliferation, cell migration, survival and differentiation by specific receptors activation. We studied its effects on L-BMAA treated neuroblastoma cells (SH-SY5Y), an amino acid that can trigger neurodegenerative diseases such as amyotrophic lateral sclerosis/Parkinson dementia complex (ALS/PDC). We found that S1P protects from necrosis and prevents the GSK3 increasing as long as the PI3K/AKT pathway is active. Moreover, GSK3 inhibition protects against neuronal death caused by L-BMAA.
- PublicationAnalysis of β-N-methylamino-l-alanine (L-BMAA) neurotoxicity in rat cerebellum(Elsevier, 2015-05) Muñoz Sáez, Emma; Munck García, Estefanía de; Arahuetes Portero, Rosa Mª; Martínez, Ana; Solas Alado, Mª Teresa; Gómez Miguel, BegoñaDue to its structural similarity to glutamate, L-BMAA could be a trigger for neurodegenerative disorders caused by changes in the intracellular medium, such as increased oxidative stress, mitochondrial dysfunction, impaired synthesis and protein degradation and the imbalance of some enzymes. It is also important to note that according to some published studies, L-BMAA will be incorporated into proteins, causing the alteration of protein homeostasis. Neuronal cells are particularly prone to suffer damage in protein folding and protein accumulation because they have not performed cellular division. In this work, we will analyse the cerebellum impairment triggered by L-BMAA in treated rats. The cerebellum is one of the most important subcortical motor centres and ensures that movements are performed with spatial and temporal precision. Cerebellum damage caused by L-BMAA can contribute to motor impairment. To characterize this neurodegenerative pathology, we first carried out ultrastructure analysis in Purkinje cells showing altered mitochondria, endoplasmic reticulum (ER), and Golgi apparatus (GA). We then performed biochemical assays of GSK3 and TDP-43 in cerebellum, obtaining an increase of both biomarkers with L-BMAA treatment and, finally, performed autophagy studies that revealed a higher level of these processes after treatment. This work provides evidence of cerebellar damage in rats after treatment with L-BMAA. Three months after treatment, affected rats cannot restore the normal functions of the cerebellum regarding motor coordination and postural control.
- PublicationDiseño y utilización de unas prácticas de Regulación del Metabolismo como herramienta integradora de conocimientos multidisciplinares en el Grado en Biología (II)(2017-01) Guillén Maestro, Alberto; Pérez Uz, María Blanca; Serrano Barrero, Susana Lourdes; Arregui García-Rovés, Lucía; Callejas Hervás, Carmen; Linacero de la Fuente, Rosario; Acebal Sarabia, Carmen; Megías Fresno, Alicia; Gómez Miguel, BegoñaSe pretende la creación de espacios multidisdiplinares en el Grado en Biología,con prácticas integradas de asignaturas que se cursan simultáneamente, que pudieran servir de base a propuestas de Trabajos de Fin de Grado.
- PublicationHerramientas de comunicación en el aprendizaje de la Bioquímica(2017-06-19) Portolés Pérez, María Teresa; Megías Fresno, Alicia; Oñaderra Sanchez, Mercedes; Aragonés Sanz, María Dolores; Martínez Díaz, Ana; Gómez Miguel, Begoña
- PublicationDesarrollo de un glosario de términos biológicos en lengua de signos para alumnos de educación secundaria y universitaria.(2015) Marquina Díaz, Domingo; Santos de la Sen, Antonio; Alonso Conde, Rafael Alejandro; Portillo Corcho, Alberto; Caballero Gómez, Ana; Arahuetes Portero, Rosa María; Pérez Gomáriz, Rosa; Carballo Cuervo, Serafín; Calvo de Pablo, Pilar; Garcia Moreno, Ana; Arriero Higueras, Elena; Gómez Miguel, Begoña; Pérez Urria Carril, Elena; Gomez Flechoso, Maria de los Angeles; Callejas Hervás, Carmen; Belda Aguilar, IgnacioEste proyecto ha permitido crear un glosario de términos biológicos en lengua de signos española. Este glosario permitirá a los alumnos sordos de enseñanza media y superior tener una mayor accesibilidad a los términos específicos de las distintas disciplinas que constituyen las Ciencias Biológicas.
- PublicationDiseño y utilización de unas prácticas de Regulación del Metabolismo como herramienta integradora de conocimientos multidisciplinares en el Grado en Biología(2015) Guillén Maestro, Alberto; Acebal Sarabia, Carmen; Callejas Hervás, Carmen; Gómez Miguel, Begoña; Linacero de la Fuente, María Rosario; Megías Fresno, Alicia; Pérez Uz, María Blanca; Serrano Barrero, Susana LourdesCon el diseño de estas prácticas de laboratorio se pretende la creación de espacios multidisdiplinares en el Grado en Biología que puedieran dar paso a un futuro modelo de prácticas integradas de asignaturas que se cursan simultáneamente.