Donepezil rescues spatial learning and memory deficits following traumatic brain injury independent of its effects on neurogenesis.
Donepezil rescues spatial learning and memory deficits following traumatic brain injury independent of its effects on neurogenesis.
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DOI：
10.1371/journal.pone.0118793
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Kernie SG
中科院分区：
文献类型：
--
作者：
Yu TS;Kim A;Kernie SG
创伤性脑损伤（TBI）是普遍存在的，有效的治疗方法，因为它仍然是支持性的，主要是由于内源性修复如何发生的不确定性。最近，我们证明海马损伤诱导的神经发生是TBI后内源性修复的一种机制。多奈哌齐与海马神经发生增加有关，长期以来一直被认为可以通过未知机制改善许多类型脑损伤后的认知的某些方面。通过使用nestin-HSV转基因小鼠将多奈哌齐治疗与损伤诱导的神经发生的时间调节消融相结合，我们研究了损伤后多奈哌齐的促认知作用是否可能通过增加神经发生而发生。我们证明，多奈哌齐本身增强神经发生和改善认知功能TBI后，即使损伤诱导的神经发生被抑制。这表明多奈哌齐在TBI中的治疗作用与其对神经发生的作用分开发生。
Traumatic brain injury (TBI) is ubiquitous and effective treatments for it remain supportive largely due to uncertainty over how endogenous repair occurs. Recently, we demonstrated that hippocampal injury-induced neurogenesis is one mechanism underlying endogenous repair following TBI. Donepezil is associated with increased hippocampal neurogenesis and has long been known to improve certain aspects of cognition following many types of brain injury through unknown mechanisms. By coupling donepezil therapy with temporally regulated ablation of injury-induced neurogenesis using nestin-HSV transgenic mice, we investigated whether the pro-cognitive effects of donepezil following injury might occur through increasing neurogenesis. We demonstrate that donepezil itself enhances neurogenesis and improves cognitive function following TBI, even when injury-induced neurogenesis was inhibited. This suggests that the therapeutic effects of donepezil in TBI occur separately from its effects on neurogenesis.
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