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路易体痴呆患者大脑视觉通路中路易病理的研究。

Investigation of Lewy pathology in the visual pathway of brains of dementia with Lewy bodies.

作者信息

Yamamoto Ryoko, Iseki Eizo, Murayama Norio, Minegishi Michiko, Marui Wami, Togo Takashi, Katsuse Omi, Kato Masanori, Iwatsubo Takeshi, Kosaka Kenji, Arai Heii

机构信息

Department of Psychiatry, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3-3-20 Shinsuna, Koto-ku, Tokyo 136-0075, Japan.

出版信息

J Neurol Sci. 2006 Jul 15;246(1-2):95-101. doi: 10.1016/j.jns.2006.02.016. Epub 2006 Apr 19.

DOI:10.1016/j.jns.2006.02.016
PMID:16624323
Abstract

We examined 19 autopsied cases of dementia with Lewy bodies (DLB) using pathological and alpha-synuclein-immunohistochemical methods, and investigated Lewy pathology in the primary visual pathway (lateral geniculate body and Brodmann's area 17), secondary visual pathway (pulvinar, Brodmann's areas 18 and 19, and inferior temporal cortex), amygdala and substantia nigra, to clarify the relationship between visual misidentification and Lewy pathology in the visual pathway. Consequently, the secondary visual pathway revealed significantly severer Lewy pathology than the primary visual pathway, suggesting that the degeneration of the secondary visual pathway induces dysfunction in the recognition of objects shape and color. In addition, the amygdala revealed significantly severer Lewy pathology and neuronal loss than the primary and secondary visual pathways, suggesting that the degeneration of the amygdala, which receives the afferent connections from the substantia nigra, fails to modulate the visual processing according to cognition and emotion. These findings suggest that Lewy pathologies in the secondary visual pathway and amygdala may cause the dysfunction of the visuo-amygdaloid pathway and participate in visual misidentification in DLB patients. In addition, we compared Lewy pathology between cases with and without visual hallucinations, and showed no significant differences between the two groups.

摘要

我们使用病理学和α-突触核蛋白免疫组织化学方法检查了19例路易体痴呆(DLB)尸检病例,并研究了初级视觉通路(外侧膝状体和布罗德曼17区)、次级视觉通路(丘脑枕、布罗德曼18区和19区以及颞下回皮质)、杏仁核和黑质中的路易体病理,以阐明视觉识别错误与视觉通路中路易体病理之间的关系。结果发现,次级视觉通路的路易体病理比初级视觉通路严重得多,这表明次级视觉通路的退化会导致物体形状和颜色识别功能障碍。此外,杏仁核的路易体病理和神经元丢失比初级和次级视觉通路严重得多,这表明接受来自黑质传入连接的杏仁核退化,无法根据认知和情感调节视觉处理。这些发现表明,次级视觉通路和杏仁核中的路易体病理可能导致视觉-杏仁核通路功能障碍,并参与DLB患者的视觉识别错误。此外,我们比较了有和没有视幻觉的病例之间的路易体病理,结果显示两组之间没有显著差异。

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Investigation of Lewy pathology in the visual pathway of brains of dementia with Lewy bodies.路易体痴呆患者大脑视觉通路中路易病理的研究。
J Neurol Sci. 2006 Jul 15;246(1-2):95-101. doi: 10.1016/j.jns.2006.02.016. Epub 2006 Apr 19.
2
Correlation in Lewy pathology between the claustrum and visual areas in brains of dementia with Lewy bodies.路易体痴呆患者大脑中屏状核与视觉区域之间路易体病理的相关性。
Neurosci Lett. 2007 Mar 30;415(3):219-24. doi: 10.1016/j.neulet.2007.01.029. Epub 2007 Jan 14.
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The nigro-striatal and nigro-amygdaloid pathways undergo different degeneration processes in brains of dementia with Lewy bodies.在路易体痴呆患者的大脑中,黑质-纹状体通路和黑质-杏仁核通路经历不同的退化过程。
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Age-associated prevalence and risk factors of Lewy body pathology in a general population: the Hisayama study.一般人群中路易体病理的年龄相关性患病率及危险因素:久山研究
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A stable proportion of Lewy body bearing neurons in the substantia nigra suggests a model in which the Lewy body causes neuronal death.黑质中存在稳定比例的路易体神经元提示路易体导致神经元死亡的模型。
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In dementia with Lewy bodies, Braak stage determines phenotype, not Lewy body distribution.在路易体痴呆中,Braak分期决定表型,而非路易小体分布。
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Clinical and biochemical correlates of insoluble alpha-synuclein in dementia with Lewy bodies.路易体痴呆中不溶性α-突触核蛋白的临床与生化相关性
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An atypical autopsy case of Lewy body disease with clinically diagnosed major depression: a clinical, radiological and pathological study.一例临床诊断为重度抑郁症的路易体病非典型尸检病例:临床、影像学及病理学研究
Neuropathology. 2008 Dec;28(6):652-9. doi: 10.1111/j.1440-1789.2008.00905.x. Epub 2008 Apr 10.

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Cortical α-synuclein pathology induces cell autonomous neuronal hypoactivity and compensatory circuit changes in a model of early Lewy body dementia.在早期路易体痴呆模型中,皮质α-突触核蛋白病变会引发细胞自主性神经元活动减退和代偿性回路变化。
bioRxiv. 2025 Aug 1:2025.07.31.668024. doi: 10.1101/2025.07.31.668024.
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Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?路易体痴呆和帕金森病痴呆——相同还是不同,这重要吗?
Nat Rev Neurol. 2025 May 12. doi: 10.1038/s41582-025-01090-x.
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Clinically probable RBD is an early predictor of malignant non-motor Parkinson's disease phenotypes.
临床疑似快速眼动睡眠行为障碍是恶性非运动性帕金森病表型的早期预测指标。
NPJ Parkinsons Dis. 2025 Jan 29;11(1):25. doi: 10.1038/s41531-025-00874-8.
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Visual dysfunction in dementia with Lewy bodies.路易体痴呆的视觉功能障碍。
Curr Neurol Neurosci Rep. 2024 Aug;24(8):273-284. doi: 10.1007/s11910-024-01349-8. Epub 2024 Jun 22.
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Pulvinar quantitative susceptibility mapping predicts visual hallucinations post-deep brain stimulation in Parkinson's disease.丘脑定量磁化率图预测帕金森病深部脑刺激术后出现幻视。
Brain Behav. 2023 Nov;13(11):e3263. doi: 10.1002/brb3.3263. Epub 2023 Sep 24.
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Optic radiation atrophy in Lewy body disease with visual hallucination on phase difference enhanced magnetic resonance images.路易体病伴视幻觉的视辐射萎缩在相位差增强磁共振图像上的表现。
Sci Rep. 2022 Nov 3;12(1):18556. doi: 10.1038/s41598-022-21847-4.
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Perception of Fragmented Letters by Patients With Pathologically Confirmed Dementia With Lewy Bodies or Alzheimer Disease.路易体痴呆症与阿尔茨海默病患者对碎片化字母的感知。
Neurology. 2022 Nov 1;99(18):e2034-e2043. doi: 10.1212/WNL.0000000000201068. Epub 2022 Aug 26.
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Low Pulvinar Intensity in Susceptibility-Weighted Imaging May Suggest Cognitive Worsening After Deep Brain Stimulation Therapy in Patients With Parkinson's Disease.帕金森病患者深部脑刺激治疗后,磁敏感加权成像中丘脑枕低信号强度可能提示认知功能恶化
Front Neurol. 2019 Oct 31;10:1158. doi: 10.3389/fneur.2019.01158. eCollection 2019.
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Molecular changes in the absence of severe pathology in the pulvinar in dementia with Lewy bodies.在路易体痴呆症中,即使在豆状核无严重病理学改变的情况下,也存在分子变化。
Mov Disord. 2018 Jul;33(6):982-991. doi: 10.1002/mds.27333. Epub 2018 Mar 23.
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Dementia with Lewy bodies and Parkinson's disease-dementia: current concepts and controversies.路易体痴呆与帕金森病痴呆:当前的概念和争议。
J Neural Transm (Vienna). 2018 Apr;125(4):615-650. doi: 10.1007/s00702-017-1821-9. Epub 2017 Dec 8.