Ager Rahasson R, Davis Joy L, Agazaryan Andy, Benavente Francisca, Poon Wayne W, LaFerla Frank M, Blurton-Jones Mathew
Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California.
Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, California.
Hippocampus. 2015 Jul;25(7):813-26. doi: 10.1002/hipo.22405. Epub 2015 Jan 8.
Alzheimer's disease (AD) is the most prevalent age-related neurodegenerative disorder, affecting over 35 million people worldwide. Pathologically, AD is characterized by the progressive accumulation of β-amyloid (Aβ) plaques and neurofibrillary tangles within the brain. Together, these pathologies lead to marked neuronal and synaptic loss and corresponding impairments in cognition. Current treatments, and recent clinical trials, have failed to modify the clinical course of AD; thus, the development of novel and innovative therapies is urgently needed. Over the last decade, the potential use of stem cells to treat cognitive impairment has received growing attention. Specifically, neural stem cell transplantation as a treatment for AD offers a novel approach with tremendous therapeutic potential. We previously reported that intrahippocampal transplantation of murine neural stem cells (mNSCs) can enhance synaptogenesis and improve cognition in 3xTg-AD mice and the CaM/Tet-DT(A) model of hippocampal neuronal loss. These promising findings prompted us to examine a human neural stem cell population, HuCNS-SC, which has already been clinically tested for other neurodegenerative disorders. In this study, we provide the first evidence that transplantation of research grade HuCNS-SCs can improve cognition in two complementary models of neurodegeneration. We also demonstrate that HuCNS-SC cells can migrate and differentiate into immature neurons and glia and significantly increase synaptic and growth-associated markers in both 3xTg-AD and CaM/Tet-DTA mice. Interestingly, improvements in aged 3xTg-AD mice were not associated with altered Aβ or tau pathology. Rather, our findings suggest that human NSC transplantation improves cognition by enhancing endogenous synaptogenesis. Taken together, our data provide the first preclinical evidence that human NSC transplantation could be a safe and effective therapeutic approach for treating AD.
阿尔茨海默病(AD)是最常见的与年龄相关的神经退行性疾病,全球有超过3500万人受其影响。在病理学上,AD的特征是大脑内β淀粉样蛋白(Aβ)斑块和神经原纤维缠结的逐渐积累。这些病变共同导致明显的神经元和突触丧失以及相应的认知障碍。目前的治疗方法以及最近的临床试验都未能改变AD的临床病程;因此,迫切需要开发新颖的创新疗法。在过去十年中,干细胞用于治疗认知障碍的潜在用途受到越来越多的关注。具体而言,神经干细胞移植作为AD的一种治疗方法提供了一种具有巨大治疗潜力的新途径。我们之前报道过,将小鼠神经干细胞(mNSCs)海马内移植可增强3xTg-AD小鼠和海马神经元丧失的CaM/Tet-DT(A)模型中的突触形成并改善认知。这些有前景的发现促使我们研究一种人类神经干细胞群体HuCNS-SC,它已经针对其他神经退行性疾病进行了临床试验。在本研究中,我们提供了首个证据,即研究级HuCNS-SCs的移植可在两种互补的神经退行性模型中改善认知。我们还证明,HuCNS-SC细胞可以迁移并分化为未成熟的神经元和神经胶质细胞,并在3xTg-AD和CaM/Tet-DTA小鼠中显著增加突触和生长相关标记物。有趣的是,老年3xTg-AD小鼠的改善与Aβ或tau病理变化无关。相反,我们的研究结果表明,人类神经干细胞移植通过增强内源性突触形成来改善认知。综上所述,我们的数据提供了首个临床前证据,表明人类神经干细胞移植可能是治疗AD的一种安全有效的治疗方法。