Transcriptomic signatures of brain regional vulnerability to Parkinson’s disease

The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas....

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Published inCommunications biology Vol. 3; no. 1; p. 101
Main Authors Keo, Arlin, Mahfouz, Ahmed, Ingrassia, Angela M. T., Meneboo, Jean-Pascal, Villenet, Celine, Mutez, Eugénie, Comptdaer, Thomas, Lelieveldt, Boudewijn P. F., Figeac, Martin, Chartier-Harlin, Marie-Christine, van de Berg, Wilma D. J., van Hilten, Jacobus J., Reinders, Marcel J. T.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 05.03.2020
Nature Publishing Group
Subjects
38/39
38/61
38/91
631/114/116
692/617/375/1718
Adolescent
Adult
Aged
Aged, 80 and over
Biochemistry, Molecular Biology
Biology
Biomedical and Life Sciences
Brain
Brain - pathology
Case-Control Studies
Databases, Genetic
Disease Progression
Dopamine
Endothelial cells
Female
Gene Expression Profiling
Genetic Association Studies
Genetic Predisposition to Disease
Genomics
Human health and pathology
Humans
Immune system
Lewy bodies
Lewy Bodies - genetics
Lewy Bodies - pathology
Life Sciences
Male
Microglia
Middle Aged
Molecular modelling
Movement disorders
Neurobiology
Neurodegenerative diseases
Neurons and Cognition
Parkinson Disease - genetics
Parkinson Disease - pathology
Parkinson's disease
Phenotype
Risk Assessment
Risk Factors
Transcriptome
Young Adult
Online AccessGet full text

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Abstract The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson’s disease: SCARB2 , ELOVL7, SH3GL2 , SNCA , BAP1 , and ZNF184 . Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson’s disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson’s disease brains. Keo et al. perform a meta-analysis of region-specific transcriptomic profiles across different Braak stages. They identify genes and modules that may be involved in the selective regional vulnerability and the progression of Parkinson’s disease.
AbstractList The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson’s disease: SCARB2, ELOVL7, SH3GL2, SNCA, BAP1, and ZNF184. Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson’s disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson’s disease brains.Keo et al. perform a meta-analysis of region-specific transcriptomic profiles across different Braak stages. They identify genes and modules that may be involved in the selective regional vulnerability and the progression of Parkinson’s disease.
The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson’s disease: SCARB2 , ELOVL7, SH3GL2 , SNCA , BAP1 , and ZNF184 . Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson’s disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson’s disease brains.
The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson's disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson's disease: SCARB2, ELOVL7, SH3GL2, SNCA, BAP1, and ZNF184. Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson's disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson's disease brains.The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson's disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson's disease: SCARB2, ELOVL7, SH3GL2, SNCA, BAP1, and ZNF184. Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson's disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson's disease brains.
The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson’s disease: SCARB2 , ELOVL7, SH3GL2 , SNCA , BAP1 , and ZNF184 . Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson’s disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson’s disease brains. Keo et al. perform a meta-analysis of region-specific transcriptomic profiles across different Braak stages. They identify genes and modules that may be involved in the selective regional vulnerability and the progression of Parkinson’s disease.
The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified transcriptomic signatures across brain regions involved in Braak Lewy body stages in non-neurological adults from the Allen Human Brain Atlas. Among the genes that are indicative of regional vulnerability, we found known genetic risk factors for Parkinson’s disease: SCARB2 , ELOVL7, SH3GL2 , SNCA , BAP1 , and ZNF184 . Results were confirmed in two datasets of non-neurological subjects, while in two datasets of Parkinson’s disease patients we found altered expression patterns. Co-expression analysis across vulnerable regions identified a module enriched for genes associated with dopamine synthesis and microglia, and another module related to the immune system, blood-oxygen transport, and endothelial cells. Both were highly expressed in regions involved in the preclinical stages of the disease. Finally, alterations in genes underlying these region-specific functions may contribute to the selective regional vulnerability in Parkinson’s disease brains.
ArticleNumber 101
Author Comptdaer, Thomas
Lelieveldt, Boudewijn P. F.
Mutez, Eugénie
Keo, Arlin
Mahfouz, Ahmed
Villenet, Celine
Meneboo, Jean-Pascal
van de Berg, Wilma D. J.
Reinders, Marcel J. T.
Chartier-Harlin, Marie-Christine
Figeac, Martin
van Hilten, Jacobus J.
Ingrassia, Angela M. T.
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  year: 2020
  text: 2020-03-05
  day: 05
PublicationDecade 2020
PublicationPlace London
PublicationPlace_xml – name: London
– name: England
PublicationTitle Communications biology
PublicationTitleAbbrev Commun Biol
PublicationTitleAlternate Commun Biol
PublicationYear 2020
Publisher Nature Publishing Group UK
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
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Snippet The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson’s disease remain poorly understood. Here, we identified...
The molecular mechanisms underlying caudal-to-rostral progression of Lewy body pathology in Parkinson's disease remain poorly understood. Here, we identified...
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SubjectTerms 38/39
38/61
38/91
631/114/116
692/617/375/1718
Adolescent
Adult
Aged
Aged, 80 and over
Biochemistry, Molecular Biology
Biology
Biomedical and Life Sciences
Brain
Brain - pathology
Case-Control Studies
Databases, Genetic
Disease Progression
Dopamine
Endothelial cells
Female
Gene Expression Profiling
Genetic Association Studies
Genetic Predisposition to Disease
Genomics
Human health and pathology
Humans
Immune system
Lewy bodies
Lewy Bodies - genetics
Lewy Bodies - pathology
Life Sciences
Male
Microglia
Middle Aged
Molecular modelling
Movement disorders
Neurobiology
Neurodegenerative diseases
Neurons and Cognition
Parkinson Disease - genetics
Parkinson Disease - pathology
Parkinson's disease
Phenotype
Risk Assessment
Risk Factors
Transcriptome
Young Adult
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Title Transcriptomic signatures of brain regional vulnerability to Parkinson’s disease
URI https://link.springer.com/article/10.1038/s42003-020-0804-9
https://www.ncbi.nlm.nih.gov/pubmed/32139796
https://www.proquest.com/docview/2376717167
https://www.proquest.com/docview/2374365633
https://hal.science/hal-04335973
https://pubmed.ncbi.nlm.nih.gov/PMC7058608
Volume 3
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