Changes in the Neurogenesis and Axonal Sprouting in the Organotypic Hippocampal Slice Culture by Aβ25–35 Treatment

نویسندگان

  • Yeon Joo Jung
  • Hui Ling Jiang
  • Kyung Eun Lee
چکیده

Neural stem cells have the capacity to self-renew, proliferate, and give rise to lineage-restricted neuronal and/or glial progenitor cells and postmitotic specialized daughter cells. Neural progenitor cells located in the subgranular zone (SGZ) of the dentate gyrus (DG) give rise to immature neurons. These then migrate to the granule cell layer, where they differentiate into granule neurons that project to the CA3 region. Here they become electrically active, and eventually become functionally integrated into preexisting hippocampal circuits (Lie et al., 2004; Picard-Riera et al., 2004; Raineteau et al., 2004). Adult hippocampal neurogenesis has been implicated in the regulation of cognition (Rola et al., 2004; Schaffer & Gage, 2004) and the cellular repair of neurons in the central nervous system (Lie et al., 2004; Picard-Riera et al., 2004; Ziabreva et al., 2006). Recent studies have suggested that endogenous neurodegenerative mechanisms are activated in the adult human brain in response to various neuronal injuries (Ziabreva et al., 2006). The stimulation of both the proliferation and differentiation of endogenous neural progenitor cells and the transplantation of exogenous neural progenitor cells into the brain are potential therapeutic strategies in neurodegenerative disorders, such as Alzheimer’s disease (AD) (Mazur-Kolecka et al., 2006). Amyloid beta (Aβ) peptide promotes synaptic dysfunction and neuronal cell death, leading to memory impairment (Mattson, 2000; Haughey et al., 2002). For this reason it is widely used for investigating the biochemical and molecular Changes in the Neurogenesis and Axonal Sprouting in the Organotypic Hippocampal Slice Culture by Aβ25–35 Treatment

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تاریخ انتشار 2012