Browsing by Subject "Spinal cord injury (SCI)"

Now showing 1 - 3 of 3
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    Characterization and Modulation of PI3K-Akt Signaling Following Contusive SCI
    (Office of the Vice Chancellor for Research, 2011-04-08) Walker, Chandler L.; Risberg, Emelie C.; Zhu, Yusheng; Liu, Naikui; Xu, Xiao-Ming
    Spinal cord injury (SCI) is devastating, with most injuries being contusive/compressive injuries at the cervical spinal level. There are two mechanisms of damage after acute contusive SCI: a primary mechanical insult to the cord, and secondary injury induced by many biological events, including inflammation and signal-mediated cell death. The extent of tissue damage correlates with functional loss after SCI, therefore it is critical to protect neural tissue for preservation of functional ability. Focusing on cellular signaling events following SCI is a promising direction of investigation, as modulation of such pathways can promote neuroprotection or regeneration following injury. Two particular signaling pathways have been highlighted as mediators of cellular survival post-central nervous system (CNS) injury, the MEK-Erk and PI3K-Akt pathways. Reducing Erk activity has been shown to promote neuroprotection and reduced reactive gliosis, while reduction of PI3K-Akt signaling likely results in initiation of cellular death. Recent studies have demonstrated promotion of regrowth of adult corticospinal (CST) neurons and protection of motor neuron atrophy by disinhibition of PI3K via PTEN deletion or knock-down in these cells. Understanding the signal pathways and mechanisms involved in different cell types, when such response occurs, and the potential interaction between pathways is essential for maximizing development of optimal approaches to treatment following SCI. This study highlights PI3K-Akt signaling involvement following injury, with future directions aimed at better understanding this pathway for targeting therapies to mediate anatomical and functional preservation and recovery following SCI.
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    Current advances in neurotrauma research: diagnosis, neuroprotection, and neurorepair
    (Wolters Kluwer, 2014) Chen, Jinhui; Shi, Riyi; Neurological Surgery, School of Medicine
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    Regeneration Through in vivo Cell Fate Reprogramming for Neural Repair
    (Frontiers Media, 2020-04-24) Tai, Wenjiao; Xu, Xiao-Ming; Zhang, Chun-Li; Neurological Surgery, School of Medicine
    The adult mammalian central nervous system (CNS) has very limited regenerative capacity upon neural injuries or under degenerative conditions. In recent years, however, significant progress has been made on in vivo cell fate reprogramming for neural regeneration. Resident glial cells can be reprogrammed into neuronal progenitors and mature neurons in the CNS of adult mammals. In this review article, we briefly summarize the current knowledge on innate adult neurogenesis under pathological conditions and then focus on induced neurogenesis through cell fate reprogramming. We discuss how the reprogramming process can be regulated and raise critical issues requiring careful considerations to move the field forward. With emerging evidence, we envision that fate reprogramming-based regenerative medicine will have a great potential for treating neurological conditions such as brain injury, spinal cord injury (SCI), Alzheimer's disease (AD), Parkinson's disease (PD), and retinopathy.