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骨骼中的帕金森病。

Parkinson's in the bone.

作者信息

Xiong Lei, Pan Jin-Xiu, Guo Hao-Han, Mei Lin, Xiong Wen-Cheng

机构信息

Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA.

Louis Stoke VA Medical Center, Cleveland, OH, 44106, USA.

出版信息

Cell Biosci. 2021 Nov 5;11(1):190. doi: 10.1186/s13578-021-00702-5.

Abstract

Patients with Parkinson's disease (PD) exhibit systemic deficits, including arthritis and osteoporosis-like symptoms. However, the questions, how the deficits in periphery organs or tissues occur in PD patients, and what are the relationship (s) of the periphery tissue deficits with the brain pathology (e.g., dopamine neuron loss), are at the beginning stage to be investigated. Notice that both PD and osteoporosis are the products of a complex interaction of genetic and environmental risk factors. Genetic mutations in numerous genes have been identified in patients either with recessive or autosomal dominant PD. Most of these PD risk genes are ubiquitously expressed; and many of them are involved in regulation of bone metabolism. Here, we review the functions of the PD risk genes in regulating bone remodeling and homeostasis. The knowledge gaps in our understanding of the bone-to-brain axis in PD development are also outlined.

摘要

帕金森病(PD)患者存在全身性缺陷,包括关节炎和类似骨质疏松的症状。然而,关于PD患者外周器官或组织中的缺陷是如何发生的,以及外周组织缺陷与脑病理学(如多巴胺神经元丧失)之间的关系如何,这些问题尚处于研究初期。需要注意的是,PD和骨质疏松都是遗传和环境风险因素复杂相互作用的产物。在隐性或常染色体显性PD患者中已鉴定出众多基因的基因突变。这些PD风险基因大多在全身广泛表达;其中许多基因参与骨代谢的调节。在此,我们综述了PD风险基因在调节骨重塑和体内平衡中的功能。同时也概述了我们在理解PD发展过程中骨-脑轴方面的知识空白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d5e/8570029/adfae1cffc85/13578_2021_702_Fig1_HTML.jpg

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