Research advances in the role of endogenous neurogenesis on neonatal hypoxic-ischemic brain damage

Abstract

Hypoxic-ischemic brain damage (HIBD) is the main cause of perinatal mortality and neurologic complications in neonates, but it remains difficult to cure due to scarce treatments and complex molecular mechanisms remaining incompletely explained. Recent, mounting evidence shows that endogenous neurogenesis can improve neonatal neurological dysfunction post-HIBD. However, the capacity for spontaneous endogenous neurogenesis is limited and insufficient for replacing neurons lost to brain damage. Therefore, it is of great clinical value and social significance to seek therapeutic techniques that promote endogenous neurogenesis, to reduce neonatal neurological dysfunction from HIBD. This review summarizes the known neuroprotective effects of, and treatments targeting, endogenous neurogenesis following neonatal HIBD, to provide available targets and directions and a theoretical basis for the treatment of neonatal neurological dysfunction from HIBD.

Dexmedetomidine alleviates cognitive impairment by promoting hippocampal neurogenesis via BDNF/TrkB/CREB signaling pathway in hypoxic–ischemic neonatal rats

“…Multiple animal studies have provided evidence that newly generated neurons originating from the dentate gyrus have the ability to migrate toward the granule cell layer and contribute to neural repair and cognitive recovery 10,11 . However, the potential of spontaneous endogenous neurogenesis for repairing and regenerating the brain is limited and insufficient to compensate for neuron loss after HIBD 12 . Therefore, enhancing hippocampal neurogenesis may serve as a promising treatment strategy for alleviating neurological deficits induced by neonatal HIBD.…”

“… 10 , 11 However, the potential of spontaneous endogenous neurogenesis for repairing and regenerating the brain is limited and insufficient to compensate for neuron loss after HIBD. 12 Therefore, enhancing hippocampal neurogenesis may serve as a promising treatment strategy for alleviating neurological deficits induced by neonatal HIBD. Brain‐derived neurotrophic factor (BDNF), a member of the neurotrophin family, is essential for the differentiation of neural stem cells (NSCs), as well as neuronal growth, maturation, and maintenance.…”