About this Research Topic
Neurogenesis from endogenous neural stem cells (NSC) persists in at least three regions of the adult mammalian brain, the hippocampus, olfactory bulb and hypophysis. Its function in normal conditions is not fully understood and is still under intense investigation. Moreover, NSC are (re)activated in pathological conditions such as neurodegenerative diseases or brain injury. The NSC can give rise to different neuronal sub-types, using a variety of neurotransmitters such as GABA, glutamate or dopamine, as well as to glial cells. The molecular control of fate determination from postnatal NSC shares many aspects with fate determination in embryonic development but also presents specific features.
Deciphering the molecular control of NSC fate determination in normal conditions will impact the general understanding of how a particular neural cell is generated. It should also generate tools to determine the functional significance of adult neurogenesis by artificially modifying specific fates and measuring the impact on animal behaviors.
Studies on the genetic control of NSC fate commitment may also have important therapeutic implications. Indeed, one could manipulate NSC fate in vivo and recruit NSC progeny for cell replacement. Alternatively, it may be possible to block unintended neurogenic reactions in response to a lesion or disease. Finally, these studies may also allow to refine the in vitro protocols of differentiation of ES /iPS cells into desired neuronal phenotype.
The aim of this research topic is to gather contributions covering all these aspects of the topic that rarely meet.
Deciphering the molecular control of NSC fate determination in normal conditions will impact the general understanding of how a particular neural cell is generated. It should also generate tools to determine the functional significance of adult neurogenesis by artificially modifying specific fates and measuring the impact on animal behaviors.
Studies on the genetic control of NSC fate commitment may also have important therapeutic implications. Indeed, one could manipulate NSC fate in vivo and recruit NSC progeny for cell replacement. Alternatively, it may be possible to block unintended neurogenic reactions in response to a lesion or disease. Finally, these studies may also allow to refine the in vitro protocols of differentiation of ES /iPS cells into desired neuronal phenotype.
The aim of this research topic is to gather contributions covering all these aspects of the topic that rarely meet.
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