Nancy Pavón Fuentes

Bio: Nancy Pavón Fuentes is an academic researcher. The author has contributed to research in topics: Pedunculopontine nucleus & Oxidative stress. The author has an hindex of 6, co-authored 17 publications receiving 132 citations.

Follow-Up of Peripheral IL-1β and IL-6 and Relation with Apoptotic Death in Drug-Resistant Temporal Lobe Epilepsy Patients Submitted to Surgery

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.

Inflammatory mediators in epilepsy.

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.

Oxidative Stress in Patients with Drug Resistant Partial Complex Seizure.

Abstract: Oxidative stress (OS) has been implicated as a pathophysiological mechanism of drug-resistant epilepsy, but little is known about the relationship between OS markers and clinical parameters, such as the number of drugs, age onset of seizure and frequency of seizures per month. The current study’s aim was to evaluate several oxidative stress markers and antioxidants in 18 drug-resistant partial complex seizure (DRPCS) patients compared to a control group (age and sex matched), and the results were related to clinical variables. We examined malondialdehyde (MDA), advanced oxidation protein products (AOPP), advanced glycation end products (AGEs), nitric oxide (NO), uric acid, superoxide dismutase (SOD), glutathione, vitamin C, 4-hydroxy-2-nonenal (4-HNE) and nitrotyrosine (3-NT). All markers except 4-HNE and 3-NT were studied by spectrophotometry. The expressions of 4-HNE and 3-NT were evaluated by Western blot analysis. MDA levels in patients were significantly increased (p ≤ 0.0001) while AOPP levels were similar to the control group. AGEs, NO and uric acid concentrations were significantly decreased (p ≤ 0.004, p ≤ 0.005, p ≤ 0.0001, respectively). Expressions of 3-NT and 4-HNE were increased (p ≤ 0.005) similarly to SOD activity (p = 0.0001), whereas vitamin C was considerably diminished (p = 0.0001). Glutathione levels were similar to the control group. There was a positive correlation between NO and MDA with the number of drugs. The expression of 3-NT was positively related with the frequency of seizures per month. There was a negative relationship between MDA and age at onset of seizures, as well as vitamin C with seizure frequency/month. We detected an imbalance in the redox state in patients with DRCPS, supporting oxidative stress as a relevant mechanism in this pathology. Thus, it is apparent that some oxidant and antioxidant parameters are closely linked with clinical variables.

Alteraciones inmunológicas en pacientes epilépticos asociadas a la localización del foco epileptogénico

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.

Neurotrophic factor therapy for Parkinson's disease.

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.

Regulation of Nerve Growth Factor Sythesis/Secretion by Catecholamine in Cultured Mouse Astroglial 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.