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首页 » 生物研究 » Neurology:牛奶中农药残留或增加帕金森病患病风险

Neurology:牛奶中农药残留或增加帕金森病患病风险

来源:生物谷 2015-12-14 10:13

图片来自:www.euractiv.com

2015年12月14日/生物谷BIOON/--最新的研究指出,在80年代初期存在于牛奶中的农药残留,可能会增加帕金森氏病的发生风险,这种风险近期开始逐渐显现出来了。研究人员们重点关注了在夏威夷的日本裔男子的脑部健康。夏威夷以前频繁使用农药,导致八十年代初期的牛奶中存在农药的残留。研究发现,平均来说,那些每天喝两杯以上牛奶的人,相对于喝牛奶较少的人,三十年来,他们脑部的黑质区域的神经元细胞少了40%。相关研究发表在《Neurology》上。

在80年代初的夏威夷,在那里的化学杀虫剂被用于控制菠萝作物上的昆虫。后来在牛奶中发现了高浓度农药的残留。根据美国环境保护署的信息,1988年在商业销售中的农药被禁止。然而,类似的化合物在今天还被用于在输电网络系统中控制害虫火蚁。

在大脑中黑质区域脑细胞的减少,可能是帕金森氏症的早期迹象,神经细胞的减少可能开始于十年前,却不会导致任何明显症状。这项研究包括了一群居住在夏威夷的平均年龄为54岁男性日本裔美国人。该此前有研究表明,抽烟的人患帕金森氏症的风险较低。研究也发现,曾经抽烟的人即使喝牛奶很多也不会出现黑质区域神经细胞的减少。

在这项研究中,研究人员随后对450位男性进行了超过30年的跟踪研究,直到他们死了,然后再解剖了他们的尸体。观察他们脑部黑质的细胞数量,并且还测量了116具尸体大脑的农药残留量。研究人员还发现,一种杀虫剂(环氧七氯),在90%常喝牛奶的男性大脑都有残留,而那些很少喝牛奶的男性只有63%的被发现该杀虫剂的残留。研究人员指出,他们没有直接的证据表明人喝了含农药牛奶。然而,他们“只是没有其他的解释了”。

这一发现表明,饮食可能在帕金森氏病的发展中起了作用。然而,新的结果不显示农药或牛奶和帕金森氏病早期迹象的之间因果关系。相反,他们只是认为这之间存在关联性。尽管如此,研究人员还是建议大家尽量减少食用有农药残留风险的食物 。(生物谷Bioon.com)

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doi: http://dx.doi.org/10.1212/WNL.0000000000002151

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PMID:

Increased CSF biomarkers of angiogenesis in Parkinson disease

Objective: To study biomarkers of angiogenesis in Parkinson disease (PD), and how these are associated with clinical characteristics, blood–brain barrier (BBB) permeability, and cerebrovascular disease.

Methods: In this cross-sectional analysis, 38 elderly controls and 100 patients with PD (82 without dementia and 18 with dementia) were included from the prospective Swedish BioFinder study. CSF samples were analyzed for the angiogenesis biomarkers vascular endothelial growth factor (VEGF); its receptors, VEGFR-1 and VEGFR-2; placental growth factor (PlGF); angiopoietin 2 (Ang2); and interleukin-8. BBB permeability, white matter lesions (WMLs), and cerebral microbleeds (CMB) were assessed. CSF angiogenesis biomarkers were also measured in 2 validation cohorts: (1) 64 controls and 87 patients with PD with dementia; and (2) 35 controls and 93 patients with neuropathologically confirmed diagnosis of PD with and without dementia.

Results: Patients with PD without dementia displayed higher CSF levels of VEGF, PlGF, and sVEGFR-2, and lower levels of Ang2, compared to controls. Similar alterations in VEGF, PlGF, and Ang2 levels were observed in patients with PD with dementia. Angiogenesis markers were associated with gait difficulties and orthostatic hypotension as well as with more pronounced BBB permeability, WMLs, and CMB. Moreover, higher levels of VEGF and PlGF levels were associated with increased CSF levels of neurofilament light (a marker of neurodegeneration) and monocyte chemotactic protein–1 (a marker of glial activation). The main results were validated in the 2 additional cohorts.

Conclusions: CSF biomarkers of angiogenesis are increased in PD, and they are associated with gait difficulties, BBB dysfunction, WMLs, and CMB. Abnormal angiogenesis may be important in PD pathogenesis and contribute to dopa-resistant symptoms.

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