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帕金森疾病或始于机体胃肠道

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 近日一项来自丹麦奥胡斯大学等处研究人员的最新研究结果表明,人类的帕金森疾病或开始于机体的胃肠道,通过迷走神经扩散到大脑,相关研究发表于国际杂志Annals of Neurology上。

  近日一项来自丹麦奥胡斯大学等处研究人员的最新研究结果表明,人类的帕金森疾病或开始于机体的胃肠道,通过迷走神经扩散到大脑,相关研究发表于国际杂志Annals of Neurology上。
  研究者Elisabeth Svensson教授指出,文章中我们对1.5万名登记的病人进行研究,这些患者机体胃部的迷走神经均被切断,在1970年至1995年间切断患者胃部的迷走神经常常会作为一种治疗溃疡的疗法,如果帕金森疾病的确始于胃肠道,随后通过迷走神经扩散到大脑,那么进行迷走神经切断术的患者就应当尽量减少迷走神经的切除,从而来保护机体抵御帕金森疾病的发生。
  文章中,研究者表示,进行整个迷走神经切除的患者往往会被保护免于换帕金森疾病的发生,患帕金森的风险在20年后会减半,仅切除一部分迷走神经的患者并不会被保护免于帕金森的发生,因此这同研究者的假设基本一致,即免于帕金森疾病的整个过程依赖于完整未受损的迷走神经,而且迷走神经能够顺利达到大脑并且影响大脑的功能。
  许多患者在确诊为帕金森疾病之前往往会经常遭受胃肠道疾病的折磨,Elisabeth Svensson指出,帕金森患者通常在他们确诊之前会多年患便秘,这或许是一种特殊标志,来指示机体神经病理学同迷走神经相关的胃肠道病理学之间的关联。此前研究者在动物和细胞研究中揭示了帕金森疾病和迷走神经之间的关系,然而本文研究则首次对人类进行了大规模的流行病学调查。
  最后研究者表示,如今我们发现胃肠道迷走神经和机体患帕金森疾病之间的重要关联,这对于后期寻找诱发机体神经变性疾病的风险因子提供了一定的帮助,同时也为开发特殊疗法来来抑制疾病的发生提供了新的希望,研究者希望通过后期研究可以更清楚地阐明迷走神经和个体患帕金森疾病之间的精细关系。(转化医学网360zhyx.com)
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转化医学网推荐的原文摘要:

Vagotomy and subsequent risk of Parkinson's disease
Annals of Neurology    DOI: 10.1002/ana.24448
Elisabeth Svensson PhD1,*, Erzsébet Horváth-Puhó PhD1, Reimar W Thomsen PhD1, Jens Christian Djurhuus DMSc2, Lars Pedersen PhD1, Per Borghammer DMSc2,3 andHenrik Toft Sørensen DMSc1
Objectives: Parkinson's disease (PD) may be caused by an enteric neurotropic pathogen entering the brain through the vagal nerve, a process that may take over 20 years. We investigated the risk of PD in patients who underwent vagotomy, and hypothesized that truncal vagotomy is associated with a protective effect, while super-selective vagotomy has a minor effect.

Methods: We constructed cohorts of all patients in Denmark who underwent vagotomy during 1977-1995 and a matched general population cohort, by linking Danish registries. We used Cox regression to compute hazard ratios (HRs) for PD and corresponding 95% confidence intervals [CIs], adjusting for potential confounders.

Results: Risk of PD was decreased in patients who underwent truncal [HR = 0.85, 95% CI= 0.56–1.27; follow-up of >20 years: HR = 0.58, 95% CI: 0.28–1.20] compared to super-selective vagotomy. Risk of PD was also decreased following truncal vagotomy when compared to the general population cohort [overall adjusted HR = 0.85, 95% CI 0.63–1.14; follow-up >20 years, adjusted HR = 0.53 [95% CI: 0.28–0.99]. In patients who underwent super-selective vagotomy, risk of PD was similar to the general population [HR = 1.09, 95% CI: 0.84–1.43; follow-up of >20 years: HR = 1.16, 95% CI: 0.80–1.70]. The statistical precision of the risk estimates was limited. Results were consistent after external adjustment for unmeasured confounding by smoking.

Interpretation: Full truncal vagotomy is associated with a decreased risk for subsequent PD, suggesting that the vagal nerve may be critically involved in the pathogenesis of PD. This article is protected by copyright. All rights reserved.


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