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Erratum: Differences in activation of ERK1/2 and p38 kinase in Jnk3 null mice following KA treatment (Journal of Neurochemistry (2010) 114 (1315-1322))
OtherAbstract:Palabras claves:Autores:Antoni Camins, Auladell C., De Lemos M.L., Ferrer I., Folch J., Junyent F., Pallás M., Romero R., Verdaguer E.Fuentes:scopusEvaluation of hypoxia inducible factor expression in inflammatory and neurodegenerative brain models
ArticleAbstract: The neuroinflammatory process is thought to contribute to the progression of neurological disordersPalabras claves:Alzheimer's, apoptosis, APP/PS1, c-Jun, HIF-1αAutores:Antoni Camins, Auladell C., Brox S., de la Torre A.V., De Lemos M.L., Folch J., Lazarowski A., Pallás M., Petrov D., Zárate C.B.Fuentes:scopusNeuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms
ArticleAbstract: The activation of c-Jun-N-terminal kinases (JNK) pathway has been largely associated with the pathogPalabras claves:c-Jun N-terminal kinase, Excitotoxicity, hippocampus, inflammation, Kainic acid, Knockout mice, Neurodegeneration, neuroprotectionAutores:Antoni Camins, Auladell C., Castro-Torres R.D., De Lemos M.L., Folch J., Junyent F., Olloquequi J., Verdaguer E., Zárate C.B.Fuentes:scopusLack of Jun-N-terminal kinase 3 (JNK3) does not protect against neurodegeneration induced by 3-nitropropionic acid
ArticleAbstract: Aims: 3-Nitropropionic acid (3-NP) is a toxin that replicates most of the clinical and pathophysioloPalabras claves:Huntington, JNK3, Neurodegeneration, Nitropropionic acidAutores:Antoni Camins, Auladell C., De Lemos M.L., Folch J., Junyent F., Pallás M., Verdaguer E., Zárate C.B.Fuentes:scopusHypercholesterolemia and neurodegeneration. Comparison of hippocampal phenotypes in LDLr knockout and APPswe/PS1dE9 mice
ArticleAbstract: Previous studies suggest that Alzheimer's disease (AD) neurobiology could not be explained solely byPalabras claves:Alzheimer's disease, APP/PS1, cholesterol, hippocampus, LDLR-/-, OXPHOSAutores:Alegret M., Antoni Camins, De Lemos M.L., Ettcheto M., Folch J., Laguna J.C., Pallás M., Pedros I., Petrov D.Fuentes:scopusMavoglurant as a treatment for Parkinson's disease
ReviewAbstract: Introduction: A major unresolved issue in the Parkinson's disease (PD) treatment is the developmentPalabras claves:L-Dopa, Mavoglurant, Mlgu5, Parkinson's DiseaseAutores:Antoni Camins, Auladell C., Canudas A.M., De Lemos M.L., Folch J., Lazarowski A., Pallás M., Pedros I., Petrov D., Zárate C.B.Fuentes:scopusMice Lacking Functional Fas Death Receptors Are Protected from Kainic Acid-Induced Apoptosis in the Hippocampus
ArticleAbstract: The Fas receptor (FasR)/Fas ligand (FasL) system plays a significant role in the process of neuronalPalabras claves:apoptosis, Caspase-3, FAS, Kainic acid, Microglia, neuroprotectionAutores:Antoni Camins, Auladell C., De Lemos M.L., Ettcheto M., Folch J., Gómez-Sintes R., Junyent F., Lucas J.J., Pallás M., Verdaguer E., Zárate C.B.Fuentes:scopusVulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis
ArticleAbstract: The pathogenesis of Alzheimer disease (AD) is characterized by accumulation of β-amyloid protein inPalabras claves:Alzheimer disease, APPswe/PS1dE9 mouse, Calbindin, Calretinin, hippocampus, ParvalbuminAutores:Antoni Camins, Auladell C., Brox S., De Lemos M.L., Olloquequi J., Petrov D., Romero R., Verdaguer E.Fuentes:scopusRole of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration
ReviewAbstract: Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decadPalabras claves:apoptosis, C-Jun N-terminal kinase signaling pathway, hippocampus, Kainic acid, neuroprotection, ReviewAutores:Antoni Camins, Auladell C., Busquets O., De Lemos M.L., Ettcheto M., Folch J., Lazarowski A., Olloquequi J., Verdaguer E., Zárate C.B.Fuentes:scopusTau hyperphosphorylation and axonal damage induced by N,N- diethyldithiocarbamate (DEDTC) treatment along late postnatal development is followed by a rescue during adulthood
ArticleAbstract: Axonal degeneration has been described as the pathological hallmark of peripheral neuropathies inducPalabras claves:Axonal damage, DEDTC, Postnatal development, Tau phosphorylationAutores:Antoni Camins, Auladell C., De Lemos M.L., Junyent F., Pallás M., Romero R., Utrera J.Fuentes:scopus