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Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans
Huang, Xiaobing1; Wang, Changliang1,2; Chen, Liang3,4; Zhang, Tianjiao1; Leung, Ka Lai1; Wong, Garry1
2021-10-01
Source PublicationBiochimica et Biophysica Acta - Molecular Basis of Disease
ISSN0925-4439
Volume1867Issue:10
Abstract

Amyloid β (Aβ), a product of APP, and SNCA (α-synuclein (α-syn)) are two of the key proteins found in lesions associated with the age-related neurodegenerative disorders Alzheimer's disease (AD) and Parkinson's disease (PD), respectively. Previous clinical studies uncovered Aβ and α-syn co-expression in the brains of patients, which lead to Lewy body dementia (LBD), a disease encompassing Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). To explore the pathogenesis and define the relationship between Aβ and α-syn for LBD, we established a C. elegans model which co-expresses human Aβ and α-syn with alanine 53 to threonine mutant (α-syn(A53T)) in pan-neurons. Compared to α-syn(A53T) single transgenic animals, pan-neuronal Aβ and α-syn(A53T) co-expression further enhanced the thrashing, egg laying, serotonin and cholinergic signaling deficits, and dopaminergic neuron damage in C. elegans. In addition, Aβ increased α-syn expression in transgenic animals. Transcriptome analysis of both Aβ;α-syn(A53T) strains and DLB patients showed common downregulation in lipid metabolism and lysosome function genes, suggesting that a decrease of lysosome function may reduce the clearance ability in DLB, and this may lead to the further pathogenic protein accumulation. These findings suggest that our model can recapitulate some features in LBD and provides a mechanism by which Aβ may exacerbate α-syn pathogenesis.

KeywordAmyloid β Lewy Body Dementia Lipid Metabolism Lysosome Function Α-synuclein
DOI10.1016/j.bbadis.2021.166203
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaBiochemistry & Molecular Biology ; Biophysics ; Cell Biology
WOS SubjectBiochemistry & Molecular Biology ; Biophysics ; Cell Biology
WOS IDWOS:000678347100016
Scopus ID2-s2.0-85109451432
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Cited Times [WOS]:3   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorWong, Garry
Affiliation1.Cancer Centre, Centre of Reproduction, Development and Aging, Faculty of Health Sciences, University of Macau, China, 999078, Macao
2.Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory), Guangzhou, 510005, China
3.Department of Computer Science, College of Engineering, Shantou University, Shantou, 515063, China
4.Key Laboratory of Intelligent Manufacturing Technology of Ministry of Education, Shantou University, Shantou, 515063, China
First Author AffilicationCentre of Reproduction, Development and Aging
Corresponding Author AffilicationCentre of Reproduction, Development and Aging
Recommended Citation
GB/T 7714
Huang, Xiaobing,Wang, Changliang,Chen, Liang,et al. Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans[J]. Biochimica et Biophysica Acta - Molecular Basis of Disease,2021,1867(10).
APA Huang, Xiaobing,Wang, Changliang,Chen, Liang,Zhang, Tianjiao,Leung, Ka Lai,&Wong, Garry.(2021).Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans.Biochimica et Biophysica Acta - Molecular Basis of Disease,1867(10).
MLA Huang, Xiaobing,et al."Human amyloid beta and α-synuclein co-expression in neurons impair behavior and recapitulate features for Lewy body dementia in Caenorhabditis elegans".Biochimica et Biophysica Acta - Molecular Basis of Disease 1867.10(2021).
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