Celulas madre y efectos secundarios.

Celulas madre (obtención) en enfermedades neurodegenerativas como parkinson u alzhaimer (como generarlas) influenciada por el aprendizaje previo o el nulo aprendizaje en relación a sus efectos secundarios (como determinarlos, uno o varios)

La hipótesis seria que la especificidad de las células dependerá de las tareas especificas a las que sea sometido el animal enfermo y sano que a su vez fomentaran el trabajo especifico de áreas bien localizadas (TAC)

Se podrían trabajar 8 grupos

La primera divisiòn será en función de la manera de ingresar las células madre al animal y cada una de ellas podrá a su vez dividirse en testigo, animal perezoso, y animal en tareas a y en tareas b.

[pic 1]   Physiol Rev 82 (3): 637-672

Copyright © 2002 by the American Physiological Society.

Physiological Reviews, Vol. 82, No. 3, July 2002, pp. 637-672; 10.1152/physrev.00004.2002. Copyright ©2002 by the American Physiological Society

Modification of Brain Aging and Neurodegenerative Disorders by Genes, Diet, and Behavior

Mark P. Mattson, Sic L. Chan, and Wenzhen Duan

Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland

Mattson, Mark P., Sic L. Chan, and Wenzhen Duan. Modification of Brain Aging and Neurodegenerative Disorders by Genes, Diet, and Behavior. Physiol. Rev. 82: 637-672, 2002.[pic 2]Multiple molecular, cellular, structural, and functional changes occur in the brain during aging. Neural cells may respond to these changes adaptively, or they may succumb to neurodegenerative cascades that result in disorders such as Alzheimer's and Parkinson's diseases. Multiple mechanisms are employed to maintain the integrity of nerve cell circuits and to facilitate responses to environmental demands and promote recovery of function after injury. The mechanisms include production of neurotrophic factors and cytokines, expression of various cell survival-promoting proteins (e.g., protein chaperones, antioxidant enzymes, Bcl-2 and inhibitor of apoptosis proteins), preservation of genomic integrity by telomerase and DNA repair proteins, and mobilization of neural stem cells to replace damaged neurons and glia. The aging process challenges such neuroprotective and neurorestorative mechanisms. Genetic and environmental factors superimposed upon the aging process can determine whether brain aging is successful or unsuccessful. Mutations in genes that cause inherited forms of Alzheimer's disease (amyloid precursor protein and presenilins), Parkinson's disease ([pic 3]-synuclein and Parkin), and trinucleotide repeat disorders (huntingtin, androgen receptor, ataxin, and others) overwhelm endogenous neuroprotective mechanisms; other genes, such as those encoding apolipoprotein E4, have more subtle effects on brain aging. On the other hand, neuroprotective mechanisms can be bolstered by dietary (caloric restriction and folate and antioxidant supplementation) and behavioral (intellectual and physical activities) modifications. At the cellular and molecular levels, successful brain aging can be facilitated by activating a hormesis response in which neurons increase production of neurotrophic factors and stress proteins. Neural stem cells that reside in the adult brain are also responsive to environmental demands and appear capable of replacing lost or dysfunctional neurons and glial cells, perhaps even in the aging brain. The recent application of modern methods of molecular and cellular biology to the problem of brain aging is revealing a remarkable capacity within brain cells for adaptation to aging and resistance to disease.

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