6533b82ffe1ef96bd1294fc8

RESEARCH PRODUCT

Chances in the Brain Cells, From Epigenetic To the Future

Soraya L. Valles

subject

Central nervous systemEpiphenomenonInflammationBiologyBioinformaticsmedicine.disease_causemedicine.anatomical_structureImmune systemBystander effectmedicineEpigeneticsNeuronmedicine.symptomNeuroscienceOxidative stress

description

Copyright: © 2014 Valles SL. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Both oxidative damage and inflammation are elevated in brain from neurodegenerative patients [1], but their pathogenic significance remains unclear. Central nervous system has its own resident immune system, in which glial cells not only serve such as supportive and nutritive roles for neuron cells, also engage in several inflammatory processes that defend the central nervous system from pathogens and help it to recover from stress and injury [2,3]. Normal glial functions can sometimes result in a serious and chronic neuro-inflammatory cycle that promotes neurodegenerative diseases, constituent a viable target for the discovery or development of neurodegenerative diseases, such as in Alzheimer’s disease protecting neurons in the mixer culture from the toxic action (Aguirre-Rueda et al., in peer review) and this point of view needs more research investigation. Astrocytes protect neurons by an increase in mitochondriogenesis thereby obtaining a better processing of oxidative stress and an efficient inflammation control (Aguirre-Rueda et al., in peer review). The importance of glial cell-propagated inflammation disorders has been seen as a bystander effect, or epiphenomenon, occurring when damaged neurons develop an activation response by glial cells. Wyss Corey and his collaborators demonstrateda phagocytosis process does it by astrocytes to eliminate and destroy Aβ peptide plates and Valles group showed antiinflammatory effects after Aβ-induction in astrocytes [2,4,5]. For us astrocytes will be the first differentiate cells to death after injury, but is difficult to kill astrocytes and these cells had been reformed by the evolution to be stronger in front of damage to protect all the cells inside our brain. That is the reason to notice astrocytes always stronger than neurons in all of the viability assays used for us and others.

https://doi.org/10.4172/2329-6682.1000e108