Winner Beate, Winkler Jürgen
IZKF Junior Research Group III, Interdisciplinary Center for Clinical Research, Nikolaus-Fiebiger Center for Molecular Medicine, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany.
Department of Molecular Neurology, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany.
Cold Spring Harb Perspect Biol. 2015 Apr 1;7(4):a021287. doi: 10.1101/cshperspect.a021287.
Adult neurogenesis is limited to specific brain regions in the mammalian brain, such as the hippocampal dentate gyrus and the subventricular zone/olfactory bulb system. Alterations in adult neurogenesis appear to be a common hallmark in different neurodegenerative diseases including Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). This is remarkable, because the distinct pathological proteins responsible for the different diseases induce the loss of different neural populations. Impaired adult neurogenesis was shown in numerous animal models of neurodegenerative diseases; however, only few postmortem studies have been performed. We will review concepts related to the interplay between cellular plasticity in regions of adult neurogenesis with a specific focus on cell-autonomous and non-cell-autonomous factors. Furthermore, various strategies aimed to stimulate neuronal plasticity will be discussed within the context of a potential translation into therapeutic approaches for neuropsychiatric symptoms associated with PD, HD, and AD.
成年神经发生仅限于哺乳动物大脑中的特定脑区,如海马齿状回和脑室下区/嗅球系统。成年神经发生的改变似乎是包括帕金森病(PD)、阿尔茨海默病(AD)和亨廷顿病(HD)在内的不同神经退行性疾病的一个共同特征。这很值得注意,因为导致不同疾病的独特病理蛋白会导致不同神经群体的丧失。在众多神经退行性疾病的动物模型中都显示出成年神经发生受损;然而,仅进行了少数尸检研究。我们将回顾与成年神经发生区域的细胞可塑性之间相互作用相关的概念,特别关注细胞自主和非细胞自主因素。此外,将在有可能转化为针对与PD、HD和AD相关的神经精神症状的治疗方法的背景下,讨论旨在刺激神经元可塑性的各种策略。