自体和异体端粒酶阳性干细胞治疗阿尔茨海默病

H. Young, M. Speight
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引用次数: 1

摘要

阿尔茨海默病是一种从现在到遥远的过去以相反的时间顺序发生的平衡和认知记忆的逐渐丧失。虽然阿尔茨海默病的病因尚不清楚,但tau蛋白的存在、β -淀粉样蛋白的聚集、激活的小胶质细胞以及神经元及其突触过程的大量损失与该疾病有关。基因似乎在阿尔茨海默病中起主要作用,但合并症也会起作用。目前已有五种药物被批准用于控制阿尔茨海默病的症状,但没有一种药物被临床证明可以改变病程或降低患阿尔茨海默病的风险。通常在初次诊断后3-9年死亡。干细胞,如胚胎干细胞、诱导多能干细胞;间充质干细胞、药物信号细胞和神经干细胞被认为是阿尔茨海默病的潜在治疗方法。虽然临床试验证明了使用这些干细胞的安全性,但没有一项试验证明对逆转阿尔茨海默病的症状有任何疗效。我们报告使用成人端粒酶阳性干细胞作为逆转AD症状的治疗方式。在一项小型队列临床试验(n=4)中,未报告任何接受治疗的个体出现不良反应。此外,端粒酶阳性干细胞在最后一次端粒酶阳性干细胞治疗4个月后,阿尔茨海默病症状的减轻效果约为50%。
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Alzheimer’s Disease Treated with Autologous and Allogeneic TelomerasePositive Stem Cells
Alzheimer’s disease is an insidious and progressive loss of balance and cognitive memories from present time to distant past that occurs in reverse chronological order. While the cause for AD is poorly understood, the presence of tau, aggregation of beta-amyloid protein, activated microglia, and massive losses of neurons and their synaptic processes have been associated with the disease. Genetics appear to play a major role in AD, but comorbidities intervene as well. There are five drug treatments approved to control the symptoms of the disease, but none were clinically proven to alter the course or decrease the risk for AD. Death eventually occurs, usually 3-9 years after initial diagnosis. Stem cells, e.g., embryonic stem cells, induced pluripotent stem cells; mesenchymal stem cells, medicinal signaling cells, and neural stem cells have been suggested as potential treatments for AD. While clinical trials demonstrated safety of administering some of these stem cells, none demonstrated any efficacy for reversing the symptoms of AD. We report the use of adult telomerase positive stem cells as a treatment modality for reversing the symptoms of AD. In a small cohort clinical trial (n=4), there were no adverse reactions reported for any individual treated. In addition, efficacy for telomerase positive stem cells approximated 50% for reduction in symptoms of Alzheimer’s disease up to four months after their last telomerase positive stem cell treatment.
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