Arai Tetsuaki, Hasegawa Masato, Akiyama Haruhiko, Ikeda Kenji, Nonaka Takashi, Mori Hiroshi, Mann David, Tsuchiya Kuniaki, Yoshida Mari, Hashizume Yoshio, Oda Tatsuro
Department of Psychogeriatrics, Tokyo Institute of Psychiatry, Setagaya-ku, Tokyo 156-8585, Japan.
Biochem Biophys Res Commun. 2006 Dec 22;351(3):602-11. doi: 10.1016/j.bbrc.2006.10.093. Epub 2006 Oct 30.
Ubiquitin-positive tau-negative neuronal cytoplasmic inclusions and dystrophic neurites are common pathological features in frontotemporal lobar degeneration (FTLD) with or without symptoms of motor neuron disease and in amyotrophic lateral sclerosis (ALS). Using biochemical and immunohistochemical analyses, we have identified a TAR DNA-binding protein of 43 kDa (TDP-43), a nuclear factor that functions in regulating transcription and alternative splicing, as a component of these structures in FTLD. Furthermore, skein-like inclusions, neuronal intranuclear inclusions, and glial inclusions in the spinal cord of ALS patients are also positive for TDP-43. Dephosphorylation treatment of the sarkosyl insoluble fraction has shown that abnormal phosphorylation takes place in accumulated TDP-43. The common occurrence of intracellular accumulations of TDP-43 supports the hypothesis that these disorders represent a clinicopathological entity of a single disease, and suggests that they can be newly classified as a proteinopathy of TDP-43.
泛素阳性、tau蛋白阴性的神经元胞质内包涵体和营养不良性神经突是伴或不伴运动神经元病症状的额颞叶痴呆(FTLD)以及肌萎缩侧索硬化症(ALS)的常见病理特征。通过生化和免疫组化分析,我们已鉴定出一种43 kDa的TAR DNA结合蛋白(TDP-43),一种在调节转录和可变剪接中起作用的核因子,作为FTLD中这些结构的一个组成部分。此外,ALS患者脊髓中的丝状包涵体、神经元核内包涵体和胶质细胞包涵体也对TDP-43呈阳性。对 Sarkosyl不溶性部分进行去磷酸化处理表明,累积的TDP-43发生了异常磷酸化。TDP-43在细胞内的累积普遍存在,这支持了这些疾病代表单一疾病临床病理实体的假说,并表明它们可被重新归类为TDP-43蛋白病。