Decreased levels of phosphorylated synuclein in plasma are correlated with poststroke cognitive impairment.

IF 5.9 2区 医学 Q2 CELL BIOLOGY Neural Regeneration Research Pub Date : 2025-09-01 Epub Date: 2024-06-03 DOI:10.4103/NRR.NRR-D-23-01348
Yi Wang, Yuning Li, Yakun Gu, Wei Ma, Yuying Guan, Mengyuan Guo, Qianqian Shao, Xunming Ji, Jia Liu
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Abstract

JOURNAL/nrgr/04.03/01300535-202509000-00022/figure1/v/2024-11-05T132919Z/r/image-tiff Poststroke cognitive impairment is a major secondary effect of ischemic stroke in many patients; however, few options are available for the early diagnosis and treatment of this condition. The aims of this study were to (1) determine the specific relationship between hypoxic and α-synuclein during the occur of poststroke cognitive impairment and (2) assess whether the serum phosphorylated α-synuclein level can be used as a biomarker for poststroke cognitive impairment. We found that the phosphorylated α-synuclein level was significantly increased and showed pathological aggregation around the cerebral infarct area in a mouse model of ischemic stroke. In addition, neuronal α-synuclein phosphorylation and aggregation were observed in the brain tissue of mice subjected to chronic hypoxia, suggesting that hypoxia is the underlying cause of α-synuclein-mediated pathology in the brains of mice with ischemic stroke. Serum phosphorylated α-synuclein levels in patients with ischemic stroke were significantly lower than those in healthy subjects, and were positively correlated with cognition levels in patients with ischemic stroke. Furthermore, a decrease in serum high-density lipoprotein levels in stroke patients was significantly correlated with a decrease in phosphorylated α-synuclein levels. Although ischemic stroke mice did not show significant cognitive impairment or disrupted lipid metabolism 14 days after injury, some of them exhibited decreased cognitive function and reduced phosphorylated α-synuclein levels. Taken together, our results suggest that serum phosphorylated α-synuclein is a potential biomarker for poststroke cognitive impairment.

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血浆中磷酸化突触核蛋白水平的降低与脑卒中后的认知障碍有关。
摘要:脑卒中后认知功能障碍是缺血性脑卒中对许多患者造成的主要继发性影响;然而,对这种情况的早期诊断和治疗却鲜有可选方案。本研究的目的是:(1)确定脑卒中后认知障碍发生过程中缺氧与α-突触核蛋白之间的具体关系;(2)评估血清磷酸化α-突触核蛋白水平是否可用作脑卒中后认知障碍的生物标志物。我们发现,在缺血性脑卒中小鼠模型中,磷酸化α-突触核蛋白水平显著升高,并在脑梗死区周围出现病理性聚集。此外,在长期缺氧的小鼠脑组织中观察到神经元α-突触核蛋白磷酸化和聚集,这表明缺氧是缺血性脑卒中小鼠脑中α-突触核蛋白介导的病理变化的根本原因。缺血性中风患者的血清磷酸化α-突触核蛋白水平明显低于健康人,并且与缺血性中风患者的认知水平呈正相关。此外,中风患者血清中高密度脂蛋白水平的降低与磷酸化α-突触核蛋白水平的降低呈显著相关。虽然缺血性脑卒中小鼠在损伤 14 天后未表现出明显的认知功能障碍或脂质代谢紊乱,但其中一些小鼠表现出认知功能下降和磷酸化 α-突触核蛋白水平降低。综上所述,我们的研究结果表明,血清磷酸化α-突触核蛋白是中风后认知障碍的潜在生物标志物。
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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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