IMR Press / FBL / Volume 12 / Issue 8 / DOI: 10.2741/2300

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Understanding our own neural stem cells in situ: can we benefit from them?

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1 Laboratorio de Investigaciones Biomedicas, University Hospital Virgen del Rocio, Seville, Spain
Front. Biosci. (Landmark Ed) 2007, 12(8), 3125–3132; https://doi.org/10.2741/2300
Published: 1 May 2007
Abstract

The discovery of endogenous adult neurogenesis within the mammalian brain has unwrapped wide expectation about the potential use of this process for nervous system repair and regeneration. Neural stem cells residing in specific niches are able to proliferate and differentiate, giving rise to migrating neuroblasts, which in turn mature into functional neurons. These new neurons integrate into the existing circuits and contribute to the structural plasticity of certain brain areas. However, recent evidence suggests that the process could become more general under pathological conditions. Adult neurogenesis increases under acute and chronic brain diseases. Neuronal precursors are directed to the lesioned areas where they contribute to tissue repair. Given this intrinsic capability of the adult brain for tissue regeneration, researchers are focusing on strategies aimed at manipulating endogenous neurogenesis to optimize therapeutic benefit. These new approaches depend on a better understanding of the physiological role of stem cells in situ, and the elucidation of the molecular cues governing neurogenesis in normal and pathological situations. In this work, I review what is actually known about the physiology of well-described adult neural stem cell populations, and how several factors defining their niches could be used to manipulate and direct the neurogenic process towards amelioration of disease.

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