Epigenetic inactivation of the autophagy–lysosomal system in appendix in Parkinson’s disease

The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA...

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Published inNature communications Vol. 12; no. 1; pp. 5134 - 18
Main Authors Gordevicius, Juozas, Li, Peipei, Marshall, Lee L., Killinger, Bryan A., Lang, Sean, Ensink, Elizabeth, Kuhn, Nathan C., Cui, Wei, Maroof, Nazia, Lauria, Roberta, Rueb, Christina, Siebourg-Polster, Juliane, Maliver, Pierre, Lamp, Jared, Vega, Irving, Manfredsson, Fredric P., Britschgi, Markus, Labrie, Viviane
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 26.08.2021
Nature Publishing Group
Nature Portfolio
Subjects
45/15
45/23
45/91
631/378
631/378/1689/1718
631/378/2584
82/58
Abnormalities
alpha-Synuclein - chemistry
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Animals
Appendix - chemistry
Appendix - metabolism
Autophagy
Brain - metabolism
Brain - pathology
Deoxyribonucleic acid
Disruption
DNA
DNA Methylation
DNA sequencing
Epigenesis, Genetic
Epigenetics
Female
Gastrointestinal system
Gastrointestinal tract
Genes
Humanities and Social Sciences
Humans
Inactivation
Lysosomes - chemistry
Lysosomes - genetics
Lysosomes - metabolism
Male
Mice
Mice, Inbred C57BL
Movement disorders
multidisciplinary
Neurodegenerative diseases
Parkinson Disease - genetics
Parkinson Disease - metabolism
Parkinson Disease - pathology
Parkinson's disease
Pathology
Phagocytosis
Protein Aggregates
Science
Science (multidisciplinary)
Synuclein
Online AccessGet full text

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Abstract The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD. Dysfunction of the gastrointestinal system, and to the autophagy lysososmal pathway (ALP) have been reported in Parkinson’s disease. Here the authors report epigenetic disruption of ALP related genes in the appendix of individuals with Parkinson’s disease.
AbstractList The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD. Dysfunction of the gastrointestinal system, and to the autophagy lysososmal pathway (ALP) have been reported in Parkinson’s disease. Here the authors report epigenetic disruption of ALP related genes in the appendix of individuals with Parkinson’s disease.
Dysfunction of the gastrointestinal system, and to the autophagy lysososmal pathway (ALP) have been reported in Parkinson’s disease. Here the authors report epigenetic disruption of ALP related genes in the appendix of individuals with Parkinson’s disease.
The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.
The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson's disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson's disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.
The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.Dysfunction of the gastrointestinal system, and to the autophagy lysososmal pathway (ALP) have been reported in Parkinson’s disease. Here the authors report epigenetic disruption of ALP related genes in the appendix of individuals with Parkinson’s disease.
ArticleNumber 5134
Author Cui, Wei
Maliver, Pierre
Marshall, Lee L.
Kuhn, Nathan C.
Lamp, Jared
Manfredsson, Fredric P.
Labrie, Viviane
Ensink, Elizabeth
Li, Peipei
Lauria, Roberta
Maroof, Nazia
Killinger, Bryan A.
Siebourg-Polster, Juliane
Rueb, Christina
Gordevicius, Juozas
Britschgi, Markus
Lang, Sean
Vega, Irving
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34446734$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson’s disease (PD). Disruption of the autophagy-lysosome...
The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson's disease (PD). Disruption of the autophagy-lysosome...
Dysfunction of the gastrointestinal system, and to the autophagy lysososmal pathway (ALP) have been reported in Parkinson’s disease. Here the authors report...
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pubmed
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StartPage 5134
SubjectTerms 45/15
45/23
45/91
631/378
631/378/1689/1718
631/378/2584
82/58
Abnormalities
alpha-Synuclein - chemistry
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Animals
Appendix - chemistry
Appendix - metabolism
Autophagy
Brain - metabolism
Brain - pathology
Deoxyribonucleic acid
Disruption
DNA
DNA Methylation
DNA sequencing
Epigenesis, Genetic
Epigenetics
Female
Gastrointestinal system
Gastrointestinal tract
Genes
Humanities and Social Sciences
Humans
Inactivation
Lysosomes - chemistry
Lysosomes - genetics
Lysosomes - metabolism
Male
Mice
Mice, Inbred C57BL
Movement disorders
multidisciplinary
Neurodegenerative diseases
Parkinson Disease - genetics
Parkinson Disease - metabolism
Parkinson Disease - pathology
Parkinson's disease
Pathology
Phagocytosis
Protein Aggregates
Science
Science (multidisciplinary)
Synuclein
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Title Epigenetic inactivation of the autophagy–lysosomal system in appendix in Parkinson’s disease
URI https://link.springer.com/article/10.1038/s41467-021-25474-x
https://www.ncbi.nlm.nih.gov/pubmed/34446734
https://www.proquest.com/docview/2564691851
https://www.proquest.com/docview/2566044158
https://pubmed.ncbi.nlm.nih.gov/PMC8390554
https://doaj.org/article/f9f6d09087434442861f49df6420270e
Volume 12
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