神经发生对阿尔茨海默病预防和恢复的治疗潜力:孕烷醇酮作为概念验证神经生成剂
Therapeutic potential of neurogenesis for prevention and recovery from Alzheimer's disease: allopregnanolone as a proof of concept neurogenic agent.
作者信息
Brinton Roberta Diaz, Wang Jun Ming
机构信息
Department of Molecular Pharmacology and Toxicology and Program in Neuroscience, Pharmaceutical Science Center, 1985 Zonal Avenue, University of Southern California, Los Angeles, CA 90033, USA.
出版信息
Curr Alzheimer Res. 2006 Jul;3(3):185-90. doi: 10.2174/156720506777632817.
A major challenge not yet addressed by current therapeutic interventions for Alzheimer's disease (AD) is the regeneration of lost neurons and neural circuitry to restore cognitive function. Therapies that lead to cessation of the degenerative process still leave the brain riddled with deteriorated neural circuits and reduced neuron number. The discovery of neurogenesis in the adult brain and the regenerative potential of neural stem cells holds the promise for restoration of neural populations and regeneration of neural circuits necessary for cerebral function. While the regenerative potential of neural stem cells is great, so too is the challenge of delivering neural stem cells to the brain. Basic science analyses and human trials indicate that constituents of microenvironments within the brain determine the neurogenic potential, phenotypic differentiation of neural stem cells and magnitude of the neural stem cell pool. Multiple analyses have documented that dentate neurogenesis is regulated by multiple growth factors which are abundant during development and which dramatically decline with age. While the cause(s) of age-associated decline in neurogenesis remains to be fully determined, loss in growth factors, FGF-2, IGF-1 and VEGF, in the microenvironment of the subgranular zone (SGZ) are prime contributors to the reduced neurogenic potential. The decline in dentate neurogenesis can be observed as early as middle age. In the aged and AD brain, both the pool of neural stem cells and their proliferative potential are markedly diminished. In parallel, the level of potential regenerative factors is diminished in the brains of Alzheimer's patients compared to age-matched controls. Our efforts have been directed towards discovery and development of small, blood brain barrier penetrant molecules to promote endogenous proliferation of neural stem cells within the brain. These endeavors have led to the discovery that the neurosteroid alloprognanolone (APalpha) is a potent and highly efficacious proliferative agent in vitro and in vivo of both rodent and human neural stem cells. Results of our in vitro studies coupled with our more recent analyses in the triple transgenic mouse model of AD suggest that APalpha is a promising strategy for promoting neurogenesis in the aged brain and potentially for restoration of neuronal populations in brains recovering from neurodegenerative disease or injury. A brief overview of issues impacting the therapeutic potential of neurogenesis and the factors used to promote neurogenesis in the aging and degenerating brain is presented. Also included is a review of our current research into the neurogenic potential of the small molecule, blood brain barrier penetrating, neurosteroid allopregnanolone (APalpha).
目前针对阿尔茨海默病(AD)的治疗干预尚未解决的一个主要挑战是使丢失的神经元和神经回路再生以恢复认知功能。那些能导致退行性过程停止的疗法,仍会使大脑中布满退化的神经回路且神经元数量减少。成人大脑中神经发生的发现以及神经干细胞的再生潜力为恢复神经群体和大脑功能所需的神经回路再生带来了希望。虽然神经干细胞的再生潜力巨大,但将神经干细胞输送到大脑的挑战也同样巨大。基础科学分析和人体试验表明,大脑内微环境的组成成分决定了神经发生潜力、神经干细胞的表型分化以及神经干细胞池的大小。多项分析已证明,齿状回神经发生受多种生长因子调节,这些因子在发育过程中丰富,但随着年龄增长会急剧下降。虽然与年龄相关的神经发生下降的原因仍有待完全确定,但颗粒下区(SGZ)微环境中生长因子FGF - 2、IGF - 1和VEGF的减少是神经发生潜力降低的主要原因。齿状回神经发生的下降早在中年时就能观察到。在老年和AD大脑中,神经干细胞池及其增殖潜力均显著降低。与此同时,与年龄匹配的对照组相比,阿尔茨海默病患者大脑中潜在再生因子的水平也有所降低。我们一直致力于发现和开发能够穿透血脑屏障的小分子,以促进大脑内神经干细胞的内源性增殖。这些努力已导致发现神经甾体别孕烯醇酮(APalpha)在体外和体内对啮齿动物及人类神经干细胞都是一种强效且高效的增殖剂。我们的体外研究结果以及最近在AD三重转基因小鼠模型中的分析表明,APalpha是促进老年大脑神经发生以及可能恢复从神经退行性疾病或损伤中恢复的大脑中神经元群体的一种有前景的策略。本文简要概述了影响神经发生治疗潜力的问题以及用于促进衰老和退化大脑中神经发生的因素。还包括对我们目前关于小分子、能穿透血脑屏障的神经甾体别孕烯醇酮(APalpha)的神经发生潜力研究的综述。