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Teresa Serrano Sánchez

Bio: Teresa Serrano Sánchez is an academic researcher from National University of Colombia. The author has contributed to research in topics: Pedunculopontine nucleus & Dopaminergic. The author has an hindex of 5, co-authored 24 publications receiving 127 citations.

Papers
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Journal ArticleDOI
TL;DR: This study examined NGF levels in the serum of healthy persons, in patients with PD and in parkinsonian rats using a double site immune-enzymatic assay (EIA) with the murine 27/21 anti-beta-NGF monoclonal antibody to reflect ongoing neurodegenerative processes in PD.

60 citations

Journal ArticleDOI
TL;DR: It was confirmed that the inflammatory alterations disappeared one year after surgery, when the majority of patients were seizure-free, and the apoptotic death process correlated with inflammation.
Abstract: Increasing amounts of evidence support the role of inflammation in epilepsy. This study was done to evaluate serum follow-up of IL-1β and IL-6 levels, as well as their concentration in the neocortex, and the relationship of central inflammation with NF-κB and annexin V in drug-resistant temporal lobe epileptic (DRTLE) patients submitted to surgical treatment. Peripheral and central levels of IL-1β and IL-6were measured by ELISA in 10 DRTLE patients. The sera from patients were taken before surgery, and 12 and 24 months after surgical treatment. The neocortical expression of NF-κB was evaluated by western blotting and annexin V co-localization with synaptophysin by immunohistochemistry. The neocortical tissues from five patients who died by non-neurological causes were used as control. Decreased serum levels of IL-1 and IL-6 were observed after surgery; at this time, 70% of patients were seizure-free. No values of IL-1 and IL-6 were detected in neocortical control tissue, whereas cytokine levels were evidenced in DRTLE. Increased NF-κB neocortex expression was found and the positive annexin V neurons were more obvious in the DRTLE tissue, correlating with IL-6 levels. The follow-up study confirmed that the inflammatory alterations disappeared one year after surgery, when the majority of patients were seizure-free, and the apoptotic death process correlated with inflammation.

31 citations

Journal ArticleDOI
TL;DR: Experimental and clinical evidence of inflammation in epilepsy is described with special emphasis on clinical aspects once the epileptogenic focus has been resected, providing insight into the complex role ofinflammatory mediators in epileptogenesis.
Abstract: All common contributing factors to epilepsy such as trauma, malignancies and infections are accompanied by different levels of central nervous system inflammation that in turn have been associated with the occurrence of seizure. Emerging data from human brain tissue and experimental models of epilepsy support the proposed involvement of inflammation in epilepsy. Key mediators of this process include, among others: interleukin (IL) -1β, IL-6, tumor necrosis factor-α, adhesion molecules and component of complement. Recent advances suggest the involvement of specific inflammatory pathways in the pathogenesis of seizures in patients with pharmacoresistant temporal lobe epilepsy, highlighting the potential for new therapeutic strategies. This review provides an overview of the current knowledge on the relationship between inflammatory mediators and epilepsy. We also describe experimental and clinical evidence of inflammation in epilepsy with special emphasis on clinical aspects once the epileptogenic focus has been resected. Further insight into the complex role of inflammation in epileptogenesis may provide new treatment options.

28 citations

Journal ArticleDOI
TL;DR: Estos resultados evidencian that existen alteraciones del sistema inmune en los pacientes epilepticos con crisis parciales complejas no asociadas al tratamiento antiepileptico.
Abstract: Objetivo. Datos clinicos y experimentales evidencian el papel del sistema inmune en la patogenia de la epilepsia. El proposito de este trabajo es mostrar los resultados de los estudios inmunologicos realizados a 30 pacientes epilepticos con crisis parciales complejas refractarias a tratamiento medico, evaluados por video-EEG. Pacientes y metodos. Los pacientes se agruparon de acuerdo con la localizacion del foco epileptogenico en: temporales (n = 16), lateralizados (n = 6) y extratemporales (n = 4). Se estudiaron, ademas, pacientes (n = 4) diagnosticados segun la evaluacion por video-EEG como epilepsia psicogena. Se determinaron los niveles de inmunoglobulinas (IgG, IgM e IgA) por inmunodifusion radial y se cuantificaron por inmunocitoquimica los linfocitos T y B (CD3 y CD20), asi como los marcadores linfocitarios: CD4, CD8, CD25 y HLA-DR. Resultados. Se evidencio un aumento significativo en el porcentaje de linfocitos T CD8+ (supresores/citotoxicos, p < 0,05) y de los marcadores de activacion CD25 (celulas receptor IL-2) y HLA-DR (antigeno leucocitario humano DR). La evaluacion de los parametros inmunologicos en los diferentes grupos de localizacion del foco epileptogenico mostro que el aumento significativo de los linfocitos CD8+ se limita a los casos temporales y lateralizados (p < 0,01). Los pacientes con localizacion extratemporal y los casos psicogenos mostraron valores normales para todos los marcadores evaluados; este ultimo grupo recibia el mismo tratamiento medico que el resto de los pacientes. Conclusiones. Estos resultados evidencian que existen alteraciones del sistema inmune en los pacientes epilepticos con crisis parciales complejas no asociadas al tratamiento antiepileptico; las mismas pueden ser factores relevantes en la patogenia de la epilepsia y guardan relacion con la localizacion del foco epileptogenico.

6 citations

01 Jan 2010
TL;DR: In this paper, Wistar et al. present a version modificada del test of the barratransversal (TBT) that permite the cuantificación del deficit motor.
Abstract: RESUMEN La degeneracion nigroestriatal que caracteriza a la enfermedad de Parkinson (EP) esestudiada en modelos experimentales en roedores por inyeccion de 6-hidroxidopamina(6-OHDA). El presente estudio presenta una version modificada del test de la barratransversal (TBT) que permite la cuantificacion del deficit motor a traves de: tiempo quedemora la rata en alcanzar una de las plataformas (latencia de escape, LE); tiempo quedemora en caer de la barra (latencia de caida, LC); numero total de errores cometidosdurante la ejecucion en cada barra (numero de errores, NE). La forma y el diametro dela seccion transversal de la barra se modificaron desde barras rectangulares y circularesde 2,5 cm de diametro hasta barras con esta misma forma y 1 cm de diametro respec-tivamente lo cual impuso la mayor dificultad a la ejecucion del test. Tres grupos deratas Wistar fueron evaluados: no-tratadas (n=15), lesionadas con 6-OHDA (n=14) yfalsas operadas (n=14). Todas las variables estudiadas mostraron diferencias signifi-cativas entre ratas controles y hemiparkinsonizadas. Para todos los tipos de barras, lasvariables LE y NE se incrementaron mientras que la LC disminuyo significativamente enlas ratas hemiparkinsonizadas en comparacion con las ratas controles. La LC mostrodiferencias altamente significativas (p<0,001) entre las barras de mayor y menordiametro. TBT es un test que explora la funcion sensoriomotora, no requiere grandessesiones de entrenamiento previo ni motivacion aversiva ni deprivacion de alimento.Este test resulta de gran utilidad para evaluar las deficiencias motoras que se presentan

6 citations


Cited by
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Journal ArticleDOI
TL;DR: A growing body of evidence supports a role for glial-produced neuroimmune factors, including the cytokine IL-6, in CNS physiology and pathology and there is a need for a greater understanding of the physiological and pathophysiological actions of IL- 6 in the CNS.

172 citations

Book ChapterDOI
TL;DR: This chapter attempts to give a brief overview on several different growth factors that have been explored for use in animal models of PD and those already used in PD patients.
Abstract: Parkinson's disease (PD) is a chronic, progressive neurodegenerative movement disorder for which there is currently no effective therapy. Over the past several decades, there has been a considerable interest in neuroprotective therapies using trophic factors to alleviate the symptoms of PD. Neurotrophic factors (NTFs) are a class of molecules that influence a number of neuronal functions, including cell survival and axonal growth. Experimental studies in animal models suggest that members of neurotrophin family and GDNF family of ligands (GFLs) have the potent ability to protect degenerating dopamine neurons as well as promote regeneration of the nigrostriatal dopamine system. In clinical trials, although no serious adverse events related to the NTF therapy has been reported in patients, they remain inconclusive. In this chapter, we attempt to give a brief overview on several different growth factors that have been explored for use in animal models of PD and those already used in PD patients.

147 citations

Furukawa, Shoei, Yoshiko, Satoyoshi, Eijiro, Hayashi, Kyozo 
30 Jun 1988
TL;DR: The results suggest that catecholamine is one of the molecules responsible for regulation of NGF synthesis/secretion in the mouse brain and other neurotransmitters tested had no effects on either growing or quiescent cells.
Abstract: The nerve growth factor (NGF) synthesis/secretion by cultured mouse astroglial cells was modulated by catecholamine. In quiescent cells, epinephrine (EN) and dopamine (DA) markedly increased the NGF content in the conditioned medium (CM). Conversely, EN, DA, and norepinephrine (NE) decreased the NGF content in growing cells. Cholinergic agonists, metacholine and carbamylcholine, slightly increased the NGF content in quiescent cells, but showed no effects on growing cells. Other neurotransmitters tested had no effects on either growing or quiescent cells. These results suggest that catecholamine is one of the molecules responsible for regulation of NGF synthesis/secretion in the mouse brain.

105 citations

Journal ArticleDOI
TL;DR: The increase in BDNF levels might reflect a compensatory mechanism against early neurodegeneration and seems to be related to inflammation, and sTNFR1 appears to mark not only the inflammatory state but also differentiates between MCI and AD, which may be an additional tool for differentiating degrees of cognitive impairment.

98 citations

Journal ArticleDOI
TL;DR: The findings suggest that CBD has a neurorestorative potential independent of NGF that might contribute to its neuroprotection against MPP(+), a neurotoxin relevant to Parkinson's disease.

80 citations