Department of Basic Medical Sciences, Faculty of Medicine, Yarmouk University, Irbid, Jordan.
Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Canada.
Curr Stem Cell Res Ther. 2023;18(5):580-594. doi: 10.2174/1574888X17666220831105257.
Alzheimer's disease (AD) is considered one of the most complicated neurodegenerative disorders, and it is associated with progressive memory loss and remarkable neurocognitive dysfunction that negatively impacts the ability to perform daily living activities. AD accounts for an estimated 60-80% of dementia cases. AD's previously known pathological basis is the deposition of amyloid β (Aβ) aggregates and the formation of neurofibrillary tangles by tau hyperphosphorylation in the cell bodies of neurons that are located in the hippocampus, neocortex, and certain other regions of the cerebral hemispheres and limbic system. The lack of neurotransmitter acetylcholine and the activation of oxidative stress cascade may also contribute to the pathogenesis of AD. These pathological events can lead to irreversible loss of neuronal networks and the emergence of memory impairment and cognitive dysfunction that can engender an abnormal change in the personality. AD cannot be cured, and to some extent, the prescribed medications can only manage the symptoms associated with this disease. Several studies have reported that the regenerative abilities of neural stem/progenitor cells (NSCs) remarkably decline in AD, which disturbs the balancing power to control its progression. Exogenous infusion or endogenous activation of NSCs may be the ultimate solution to restore the neuronal networks in the brain of AD patients and regenerate the damaged areas responsible for memory and cognition. In this mini-review, we will touch upon the fate of NSCs in AD and the utilization of neurogenesis using modified NSCs to restore cognitive functions in AD.
阿尔茨海默病（AD）被认为是最复杂的神经退行性疾病之一，它与进行性记忆丧失和显著的神经认知功能障碍有关，这些障碍会严重影响日常生活活动的能力。AD 约占痴呆症病例的 60-80%。AD 的先前已知的病理基础是淀粉样β（Aβ）聚集物的沉积和神经元细胞体中tau 过度磷酸化形成的神经原纤维缠结，这些神经元位于海马体、新皮质和大脑半球和边缘系统的某些其他区域。神经递质乙酰胆碱的缺乏和氧化应激级联的激活也可能导致 AD 的发病机制。这些病理事件可导致神经元网络的不可逆转损失，以及记忆障碍和认知功能障碍的出现，从而导致人格的异常变化。AD 无法治愈，在某种程度上，规定的药物只能治疗与这种疾病相关的症状。有几项研究报告称，AD 中神经干细胞/祖细胞（NSCs）的再生能力显著下降，这破坏了控制其进展的平衡能力。外源性输注或内源性激活 NSCs 可能是恢复 AD 患者大脑中神经元网络并再生负责记忆和认知的受损区域的最终解决方案。在这篇迷你综述中，我们将探讨 NSCs 在 AD 中的命运以及利用经过修饰的 NSCs 进行神经发生来恢复 AD 中的认知功能。
