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Role of the cycad neurotoxin BMAA in the amyotrophic lateral sclerosis-parkinsonism dementia complex of the western Pacific.

作者信息

Duncan M W

机构信息

Clinical Neurosciences Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892.

出版信息

Adv Neurol. 1991;56:301-10.

PMID:1853765
Abstract
摘要

相似文献

1
Role of the cycad neurotoxin BMAA in the amyotrophic lateral sclerosis-parkinsonism dementia complex of the western Pacific.
Adv Neurol. 1991;56:301-10.
2
2-Amino-3-(methylamino)-propanoic acid (BMAA) in cycad flour: an unlikely cause of amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.苏铁面粉中的2-氨基-3-(甲氨基)丙酸(BMAA):关岛肌萎缩侧索硬化症和帕金森痴呆综合征不太可能的病因。
Neurology. 1990 May;40(5):767-72. doi: 10.1212/wnl.40.5.767.
3
Animal models of BMAA neurotoxicity: a critical review.β-甲基氨基丙氨酸(BMAA)神经毒性的动物模型:一项批判性综述。
Life Sci. 2008 Jan 30;82(5-6):233-46. doi: 10.1016/j.lfs.2007.11.020. Epub 2007 Dec 7.
4
beta-Methylamino-L-alanine (BMAA) and amyotrophic lateral sclerosis-parkinsonism dementia of the western Pacific.β-甲基氨基-L-丙氨酸(BMAA)与西太平洋肌萎缩侧索硬化症-帕金森病痴呆综合征
Ann N Y Acad Sci. 1992 May 11;648:161-8. doi: 10.1111/j.1749-6632.1992.tb24534.x.
5
Previous studies underestimate BMAA concentrations in cycad flour.先前的研究低估了苏铁面粉中β-甲基氨基丙氨酸(BMAA)的浓度。
Amyotroph Lateral Scler. 2009;10 Suppl 2:41-3. doi: 10.3109/17482960903273528.
6
Cycads and amyotrophic lateral sclerosis/parkinsonism dementia.苏铁与肌萎缩侧索硬化症/帕金森病痴呆症
Lancet. 1988 Nov 5;2(8619):1079. doi: 10.1016/s0140-6736(88)90099-2.
7
Lathyrism and western Pacific amyotrophic lateral sclerosis: etiology of short and long latency motor system disorders.山黧豆中毒与西太平洋肌萎缩侧索硬化症:短期和长期潜伏期运动系统疾病的病因
Adv Neurol. 1991;56:287-99.
8
BMAA selectively injures motor neurons via AMPA/kainate receptor activation.β-甲基氨基丙氨酸(BMAA)通过激活α-氨基-3-羟基-5-甲基-4-异恶唑丙酸/海人藻酸(AMPA/kainate)受体选择性损伤运动神经元。
Exp Neurol. 2006 Sep;201(1):244-52. doi: 10.1016/j.expneurol.2006.04.017. Epub 2006 Jun 9.
9
beta-N-methylamino-l-alanine induces oxidative stress and glutamate release through action on system Xc(-).β-N-甲基氨基-L-丙氨酸通过作用于Xc(-)系统诱导氧化应激和谷氨酸释放。
Exp Neurol. 2009 Jun;217(2):429-33. doi: 10.1016/j.expneurol.2009.04.002. Epub 2009 Apr 15.
10
Return of the cycad hypothesis - does the amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC) of Guam have new implications for global health?苏铁假说的回归——关岛的肌萎缩侧索硬化症/帕金森病痴呆综合征(ALS/PDC)对全球健康有新的启示吗?
Neuropathol Appl Neurobiol. 2005 Aug;31(4):345-53. doi: 10.1111/j.1365-2990.2005.00686.x.

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The usage and advantages of several common amyotrophic lateral sclerosis animal models.几种常见肌萎缩侧索硬化症动物模型的应用及优势
Front Neurosci. 2024 Feb 26;18:1341109. doi: 10.3389/fnins.2024.1341109. eCollection 2024.
2
Experimental evidence challenges the presumed defensive function of a "slow toxin" in cycads.实验证据对苏铁中“慢毒素”的假定防御功能提出了挑战。
Sci Rep. 2022 Apr 9;12(1):6013. doi: 10.1038/s41598-022-09298-3.
3
BMAA extraction of cyanobacteria samples: which method to choose?蓝藻样本的β-甲基氨基丙氨酸(BMAA)提取:该选择哪种方法?
Environ Sci Pollut Res Int. 2016 Jan;23(1):338-50. doi: 10.1007/s11356-015-5266-0. Epub 2015 Aug 26.
4
Quantification of neurotoxin BMAA (β-N-methylamino-L-alanine) in seafood from Swedish markets.瑞典市场上海洋食品中神经毒素BMAA(β-N-甲基氨基-L-丙氨酸)的定量分析。
Sci Rep. 2014 Nov 6;4:6931. doi: 10.1038/srep06931.
5
Development and application of a comprehensive two-dimensional gas chromatography with time-of-flight mass spectrometry method for the analysis of L-beta-methylamino-alanine in human tissue.发展并应用全二维气相色谱飞行时间质谱法分析人组织中的 L-β-甲基氨基-L-丙氨酸。
J Chromatogr A. 2010 Jul 2;1217(27):4639-47. doi: 10.1016/j.chroma.2010.04.065. Epub 2010 May 17.
6
Neurodegenerative diseases: neurotoxins as sufficient etiologic agents?神经退行性疾病:神经毒素是充分的病因吗?
Neuromolecular Med. 2008;10(1):1-9. doi: 10.1007/s12017-007-8016-8. Epub 2007 Nov 6.
7
A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam.关岛生物放大蓝藻神经毒素的缓释机制与神经退行性疾病
Proc Natl Acad Sci U S A. 2004 Aug 17;101(33):12228-31. doi: 10.1073/pnas.0404926101. Epub 2004 Aug 4.
8
Molecular mechanisms regulating motor neuron development and degeneration.调节运动神经元发育和退化的分子机制。
Mol Neurobiol. 1999 Jun;19(3):205-28. doi: 10.1007/BF02821714.