Rehabilitating a brain with Alzheimer’s: a proposal

Alzheimer’s disease (AD) is the most common neurodegenerative disorder, originating sporadically in the population aged over 65 years, and advanced age is the principal risk factor leading to AD development. In spite of the large amount of research going on around the globe and all the information now available about AD, there is still no origin or triggering process known so far. Drugs approved for the treatment of AD include tacrine, donepezil, rivastigmine, galantamine, and memantine. These may delay or slow down the degenerative process for a while, but they can neither stop nor reverse its progression. Because that this might be due to a lack of effect of these drugs on degenerating neurons, even when they are able to potentiate the brain in nondegenerative conditions, we propose here an alternative therapy consisting of initial repair of neuronal membranes followed by conventional drug therapies. The rehabilitation of neurons in a degeneration process would enable the drugs to act more effectively on them and improve the effects of treatment in AD patients

¿Cuál es el mejor modelo de estudio de la enfermedad de Azheimer?

El problema que plantea el estudio de la enfermedad de Alzheimer, aparte de ser una enfermedad multigénica, es que no se tiene un modelo de estudio ya sea in vivo o in vitro que nos permita entender, de manera factible, como es que se inicia la enfermedad. Los modelos hasta ahora propuestos son ratas o ratones transgénicos, sin embargo éstos a lo largo de la vida no presentaran todas las característica de la enfermedad, lo mismo sucede con los cultivos celulares. Es necesario que se acepte y se defina la enfermedad en estos modelo

¿Cuál es el mejor modelo de estudio de la enfermedad de Alzheimer?

A problematic in the study of Alzheimer's disease is the lack of a good model that allows us either in vivo or in vitro to understand how the disease initiates. So far, the proposed models are mainly transgenic mice or rats, however, along their lifetime they do not present all the features of this disease and cell cultures present this same problematic. Thus, we have felt the need to define Alzheimer�s disease in acceptable models able to present all the characteristic events taking place in the pathogenesis of Alzheimer�s that until now we can only observe in postmortem analysis.El problema que plantea el estudio de la enfermedad de Alzheimer, aparte de ser una enfermedad multigénica, es que no se tiene un modelo de estudio ya sea in vivo o in vitro que nos permita entender, de manera factible, como es que se inicia la enfermedad. Los modelos hasta ahora propuestos son ratas o ratones transgénicos, sin embargo éstos a lo largo de la vida no presentaran todas las característica de la enfermedad, lo mismo sucede con los cultivos celulares. Es necesario que se acepte y se defina la enfermedad en estos modelos y que cumplan con las características que hasta ahora solo ofrecen los estudios post-mortem

Effects of electrical stimulation on WGA-HRP transport in pubococcygeus motoneurons of male rats

Introduction: The retrograde axonal transport from dendrites and the axon terminal to the soma is very important mechanism for transferring contents among the different regions of the neuron. However, the correlation between tracers labeling on motoneurons with neural electrical activity is somewhat debatable. Objetives: Therefore, we used horseradish peroxidase conjugated to wheat germ agglutinin (WGA-HRP) to analyze spinal motoneurons of the Pubococcygeus (Pc) muscle in male rats that received electrical stimulation on the left somatomotor branch of the pelvic nerve. Materials and Methods: Three groups were made according to the timing of stimulation: A) after injection of WGA-HRP, B) before perfusion of the rat, and C) both conditions, A+B. Results: The results indicated that motoneurons located on the ipsilateral side of stimulation applied twice (group C) obtained the lower values of morphological labeling. Conclusions: We suggested that the electrical activity of a motoneuron results in an increase of dendritic movement to concentrate substances in the soma, which indeed regulates WGA-HRP labeling. It is suggested that the state of electrical activity of a motoneuron increases the centripetal movement of cytoplasmic contents, as represented by the stain. The mechanism could serve to maintain the integrity of the different regions of the motoneuron by allowing recycling, degradation or transferring of components into the soma.Introducción: El transporte axonal retrógrado desde las dendritas y de terminales axónicas hacia el soma es un mecanismo importante para obtener información del cuerpo celular a las dendritas y terminales nerviosas. La correlación entre el marcaje de trazadores sobre motoneuronas con la actividad eléctrica neuronal es algo debatible. Objetivos: Por lo tanto, usamos la peroxidada de rábano conjugada con germen de trigo aglutinado (WGA-HRP) para analizar motoneuronas espinales del músculo Pubococcígeo (Pc) en ratas macho que recibieron estimulación eléctrica de la rama somatomotora izquierda del nervio pélvico. Material y Métodos: Tres grupos fueron usados de acuerdo al tiempo de estimulación: A) después de la inyección de la WGA-HRP, B) antes de la perfusión de la rata, C) ambas condiciones, A+B. Resultados: Los resultados indicaron que las motoneuronas localizadas del mismo lado de la estimulación aplicada dos veces (grupo C) obtuvieron los valores más bajos del marcaje morfológico. Conclusiones: Sugerimos, que la actividad eléctrica de una motoneurona resulta en un aumento del movimiento dendrítico para concentrar substancias en el soma, el cual realmente regula el marcaje de la WGA-HRP. Esto sugiere que estado de la actividad eléctrica de una motoneurona aumenta el movimiento centrípeto del contenido citosplásmico, representado por la tinción. El mecanismo podría servir para mantener la integridad de regiones diferentes de la motoneurona para permitir el reciclaje, la degradación o la transferencia de componentes al soma

Current Opinion on the Use of c-Fos in Neuroscience

For years, the biochemical processes that are triggered by harmful and non-harmful stimuli at the central nervous system level have been extensively studied by the scientific community through numerous techniques and animal models. For example, one of these techniques is the use of immediate expression genes, which is a useful, accessible, and reliable method for observing and quantifying cell activation. It has been shown that both the c-fos gene and its protein c-Fos have rapid activation after stimulus, with the length of time that they remain active depending on the type of stimulus and the activation time depending on the stimulus and the structure studied. Fos requires the participation of other genes (such as c-jun) for its expression (during hetero-dimer forming). c-Fos dimerizes with c-Jun protein to form factor AP-1, which promotes the transcription of various genes. The production and removal of c-Fos is part of cellular homeostasis, but its overexpression results in increased cell proliferation. Although Fos has been used as a marker of cellular activity since the 1990s, which molecular mechanism participates in the regulation of the expression of this protein is still unknown because the gene and the protein are not specific to neurons or glial cells. For these reasons, this work has the objective of gathering information about this protein and its use in neuroscience