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首页> 外文期刊>Journal of Alzheimer's disease: JAD >TMEM230 Accumulation in Granulovacuolar Degeneration Bodies and Dystrophic Neurites of Alzheimer's Disease
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TMEM230 Accumulation in Granulovacuolar Degeneration Bodies and Dystrophic Neurites of Alzheimer's Disease

机译:TMEM230在甘蓝甲酸的颗粒病变造成体内和阿尔茨海默病的营养不良神经疾病中的积累

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摘要

Transmembrane Protein 230 (TMEM230) is a newly identified protein associated with Parkinson's disease (PD) found in Lewy bodies and Lewy neurites of patients with PD or dementia with Lewy body disease. However, TMEM230 has not yet been investigated in the most common neurodegenerative disorder, Alzheimer's disease (AD). Here, we demonstrate that the expression of TMEM230 is specifically increased in neurons in AD patients. Importantly, both granulovacuolar degeneration (GVD) and dystrophic neurites (DNs), two prominent characteristic pathological structures associated with AD, contain TMEM230 aggregates. TMEM230 immunoreactivity can be detected in neurofibrillary tangles-containing neurons and hyperphosphorylated tau positive DNs. TMEM230 accumulation is also noted around senile plaques. These findings identifying TMEM230 as a component of GVD and DNs suggest TMEM230 dysregulation as a likely mechanism playing an important role in the pathogenesis of AD.
机译:跨膜蛋白230(TMEM230)是与帕金森病(PD)相关的新鉴定的蛋白质,在Lewy体和患有Lewy身体疾病的PD或痴呆患者的患者的Lewy患者中发现。 然而,TMEM230尚未在最常见的神经变性障碍中进行研究,阿尔茨海默病(AD)。 在这里,我们证明TMEM230的表达在AD患者的神经元中特异性增加。 重要的是,甘蓝丙基退化(GVD)和营养不良神经癖(DNS),与AD相关的两个突出的特征病理结构含有TMEM230聚集体。 TMEM230免疫反应可在含神经纤维缠结的神经元和高磷酸化TAU阳性DNS中检测到免疫反应性。 在老年斑块周围也注明了TMEM230积累。 这些调查结果识别TMEM230作为GVD和DNS的组件,表明TMEM230失去扫描作为在广告的发病机制中发挥着重要作用的可能机制。

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