Coricogénesis y neurodegeneración: implicaciones de la vía de la reelina en la patogenia de la enfermedad de Alzheimer.

The reelin pathway regulates interactions between migrating neurons and radial glia. The activation of this pathway is fundamental during the process of normal corticogénesis. The reelin pathway influences the cytoskeleton dynamics as well as the neural mechanisms of learning and memory and it may also play a critical role during neurodegenerative events. The reelin pathway may be disrupted by oxidative stress, excitotoxicity and other cellular anomalies caused by endogenous and exogenous factors. When disrupted, cytoskeleton components are inefficiently processed giving place to the protein aggregates that characterize Alzheimer's disease. Such aggregates have been associated with the activation of the apoptotic cascade. Neuritic plaques and neurofibrillary tangles are not innocuous byproducts of neurodegeneration, since their presence induces neuroinflammation, cell death and cognitive impairment. However, it is possible that the clinical picture of Alzheimer's disease is perpetuated, but not initially caused by these protein aggregates. Elements of the Reelin pathway could represent targets of neuronal vulnerability mediating degenerative changes in the cortical pathways associated to Alzheimer's disease. Characterization of the reelin pathway could improve the understanding of the interactions between the risk factors associated with Alzheimer's disease and could facilitate the development of novel and effective neuroprotective interventions. [ABSTRACT FROM AUTHOR]