Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.
Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.
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DOI：
10.1186/s12883-017-0956-5
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发表时间：
2017-09-06
期刊：
影响因子：
2.6
通讯作者：
Matías-Guiu J
中科院分区：
文献类型：
--
作者：
Galán L;Gómez-Pinedo U;Guerrero A;García-Verdugo JM;Matías-Guiu J
成人神经发生至少在经典的神经发生小生境中持续一生。神经发生先前已被描述为在神经退行性疾病中减少。关于肌萎缩侧索硬化症（ALS）中成人神经发生是否发生改变的知识还不多。所有以前的出版物都研究了ALS SOD 1（超氧化物歧化酶）转基因小鼠模型。本研究的目的是检查肌萎缩侧索硬化（ALS）患者（包括伴（ALS-FTD）和不伴额颞叶痴呆（FTD）的患者）经典龛（齿状回脑室下区[SVZ]和颗粒下区[SGZ]）中的成人神经发生过程。我们研究了9例ALS患者（包括2例ALS-FTD）和4例对照者的尸检。ALS经组织学证实。使用增殖标记物（Ki-67、PCNA）、多能神经祖细胞（GFAPδ）、成神经细胞（PSA-NCAM、DCX、TUJ 1）和星形胶质细胞标记物（GFAP）进行SVZ和SGZ的研究。采用非参数检验对结果进行分析。然后，我们研究了不同标记物与磷酸化TDP-43（pTDP-43）百分比之间的相关性。我们观察到所有ALS患者SVZ的增殖在统计学上显著增加。虽然这种增加在与痴呆相关的ALS形式中更为明显，但小样本量不允许进行统计亚组分析。相反，所有患者的SGZ增殖均降低。这些变化与SVZ中pTDP-43的百分比呈正相关，与SGZ中的百分比呈负指数相关。我们观察了ALS患者典型成人神经源性龛中神经祖细胞增殖的改变。2个神经原性小生境表现出相反的变化，如增殖增加的SVZ和SGZ减少。本文的在线版本（10.1186/s12883-017-0956-5）包含补充材料，可供授权用户使用。
Adult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD). We studied 9 autopsies of patients with ALS (including 2 with ALS-FTD) and 4 controls. ALS was confirmed histologically. Studies of the SVZ and SGZ were conducted using markers of proliferation (Ki-67, PCNA), of pluripotent neural progenitor cells (GFAPδ), neuroblasts (PSA-NCAM, DCX, TUJ1), and an astrocyte marker (GFAP). Results were analyzed with non-parametric tests. We then studied correlations between the different markers and the percentage of phosphorylated TDP-43 (pTDP-43). We observed a statistically significant increase in proliferation in the SVZ in all patients with ALS. While this increase was more marked in ALS forms associated with dementia, the small sample size does not permit a statistical subgroup analysis. In contrast, proliferation in the SGZ was decreased in all patients. These alterations showed a positive and direct correlation with the percentage of pTDP-43 in the SVZ, and a negative, exponential correlation with that percentage in the SGZ. We observed alterations of the proliferation of neural progenitor in classic adult neurogenic niches in patients with ALS. The 2 neurogenic niches exhibited opposite changes such that proliferation increased in the SVZ and decreased in the SGZ. The online version of this article (10.1186/s12883-017-0956-5) contains supplementary material, which is available to authorized users.
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