The mature mammalian central nervous system (CNS) is composed of three major neural cell types: neurons, astrocytes and oligodendrocytes. See MoreNeurons, of which there are many different subtypes, transmit information through action potentials and neurotransmitters. Astrocytes and oligodendrocytes (types of glial cells) provide critical support for optimal neuronal function and survival. Studying the lesser-known, but equally important roles, of glial cells has emerged as an exciting research field in the neuroscience community.
For a long time it was thought that the adult mammalian CNS was incapable of generating new neurons, making it near-impossible to repair tissue damage caused by disease or injury. Now, there is strong evidence that multipotent neural stem cells do exist in the mature mammalian CNS. This discovery has fuelled a new era of research into understanding the tremendous potential these cells hold for treatment of CNS diseases and injuries. Multipotent neural stem-like cells have also been successfully isolated from different grades and types of brain tumors, supporting the stem cell hypothesis of cancer.
Traditionally, rodents have been popular model organisms for neurological disease research, owing to the difficulty of obtaining human brain tissue for experimental studies; however, because of differences in brain development and signaling pathways, these animal models may not be fully representative of human disease pathology. Consequently, researchers have begun to use human pluripotent stem cells (hPSCs), including human embryonic stem (ES) cells and induced pluripotent stem cells (iPS cells), to generate more representative models for studyingLess
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ASCL1 Reorganizes Chromatin to Direct Neuronal Fate and Suppress Tumorigenicity of Glioblastoma Stem Cells
Investigators showed that a large subset of patient-derived glioblastoma stem cells express high levels of Achaete-scute homolog 1 (ASCL1), a proneural transcription factor involved in normal neurogenesis.Neural Cell News Volume 11.28, July 19, 2017. Read full issue at