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神经退行性疾病中的病毒:不只是犯罪的嫌疑犯。

Viruses in neurodegenerative diseases: More than just suspects in crimes.

机构信息

Institut NeuroMyoGène INMG-PGNM, Physiopathologie et Génétique du Neurone et du Muscle, UMR5261, Inserm U1315, Université Claude Bernard UCBL-Lyon1, Faculté de Médecine Rockefeller, Lyon, France.

German Center for Neurodegenerative Diseases Bonn (DZNE), Bonn, Germany.

出版信息

PLoS Pathog. 2022 Aug 4;18(8):e1010670. doi: 10.1371/journal.ppat.1010670. eCollection 2022 Aug.


DOI:10.1371/journal.ppat.1010670
PMID:35925897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9352104/
Abstract

Neurodegenerative diseases (NDs) such as Alzheimer's and Parkinson's disease are fatal neurological diseases that can be of idiopathic, genetic, or even infectious origin, as in the case of transmissible spongiform encephalopathies. The etiological factors that lead to neurodegeneration remain unknown but likely involve a combination of aging, genetic risk factors, and environmental stressors. Accumulating evidence hints at an association of viruses with neurodegenerative disorders and suggests that virus-induced neuroinflammation and perturbation of neuronal protein quality control can be involved in the early steps of disease development. In this review, we focus on emerging evidence for a correlation between NDs and viral infection and discuss how viral manipulations of cellular processes can affect the formation and dissemination of disease-associated protein aggregates.

摘要

神经退行性疾病(NDs),如阿尔茨海默病和帕金森病,是致命的神经疾病,可能有特发性、遗传性,甚至传染性病因,如传染性海绵状脑病。导致神经退行性变的病因尚不清楚,但可能涉及衰老、遗传风险因素和环境应激因素的综合作用。越来越多的证据表明病毒与神经退行性疾病之间存在关联,并提示病毒诱导的神经炎症和神经元蛋白质量控制的紊乱可能参与疾病发展的早期阶段。在这篇综述中,我们重点介绍了 NDs 与病毒感染之间相关性的新证据,并讨论了病毒对细胞过程的操纵如何影响疾病相关蛋白聚集体的形成和传播。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fac/9352104/92f86c51dda3/ppat.1010670.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fac/9352104/92f86c51dda3/ppat.1010670.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fac/9352104/92f86c51dda3/ppat.1010670.g001.jpg

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Causal effect of infectious mononucleosis on neurodegenerative diseases: A Mendelian randomization study.

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[2]
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The age-dependent neuroglial interaction with peripheral immune cells in coronavirus-induced neuroinflammation with a special emphasis on COVID-19.

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Environmental exposures and familial background alter the induction of neuropathology and inflammation after SARS-CoV-2 infection.

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[9]
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[10]
Current insights and assumptions on α-synuclein in Lewy body disease.

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本文引用的文献

[1]
COVID-19 and Neurodegenerative Diseases: Prion-Like Spread and Long-Term Consequences.

J Alzheimers Dis. 2022

[2]
VALZ-Pilot: High-dose valacyclovir treatment in patients with early-stage Alzheimer's disease.

Alzheimers Dement (N Y). 2022-3-14

[3]
Disease-Modifying Therapies for Alzheimer's Disease: More Questions than Answers.

Neurotherapeutics. 2022-1

[4]
Clearance or Hijack: Universal Interplay Mechanisms Between Viruses and Host Autophagy From Plants to Animals.

Front Cell Infect Microbiol. 2021

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Interaction between coxsackievirus B3 infection and α-synuclein in models of Parkinson's disease.

PLoS Pathog. 2021-10

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Highly efficient intercellular spreading of protein misfolding mediated by viral ligand-receptor interactions.

Nat Commun. 2021-10-19

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The Role of Viral Proteins in the Regulation of Exosomes Biogenesis.

Front Cell Infect Microbiol. 2021-5-13

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Neurotropic influenza A virus infection causes prion protein misfolding into infectious prions in neuroblastoma cells.

Sci Rep. 2021-5-12

[9]
HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons.

Autophagy. 2021-7

[10]
Inhibition of HERV-K (HML-2) in amyotrophic lateral sclerosis patients on antiretroviral therapy.

J Neurol Sci. 2021-4-15

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