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Immunogenetics of Parkinson's disease

Swanberg, Maria LU and Jimenez-Ferrer, Itzia LU (2018) p.27-44
Abstract
Inflammation is a key feature of Parkinson’s disease (PD). In postmortem PD brains, microglial activation and enhanced major histocompatibility class II (MHCII) expression are seen concomitant to the accumulation of alpha-synuclein (α-synuclein) and loss of dopaminergic cells in the substantia nigra. Recent findings showed that α-synuclein epitopes can be presented and recognized by T-cells. PD is not a single disorder; rather, it encompasses a range of clinical, epidemiological, and genetic subtypes. Around 10% of the cases have a monogenic origin, and several of the disease-causing mutations are linked to inflammatory processes. The remaining 90% of the cases are complex, where environmental and genetic risk factors synergize to induce... (More)
Inflammation is a key feature of Parkinson’s disease (PD). In postmortem PD brains, microglial activation and enhanced major histocompatibility class II (MHCII) expression are seen concomitant to the accumulation of alpha-synuclein (α-synuclein) and loss of dopaminergic cells in the substantia nigra. Recent findings showed that α-synuclein epitopes can be presented and recognized by T-cells. PD is not a single disorder; rather, it encompasses a range of clinical, epidemiological, and genetic subtypes. Around 10% of the cases have a monogenic origin, and several of the disease-causing mutations are linked to inflammatory processes. The remaining 90% of the cases are complex, where environmental and genetic risk factors synergize to induce PD pathology. To date, 41 genetic loci have been identified in genome-wide association studies as associated with PD risk, and among these, two are within the HLA region, coding for immune genes including MHCII. Thus, genetic and immune findings indicate that the immune system has a role in the etiology of PD. Experimentally, inflammatory stimuli can cause selective nigral cell loss in preclinical models of PD, and MHCII is required to elicit α-synuclein-induced pathology in mice. In this chapter, we focus on immunogenetics, that is, the relation between genetic risk factors and immune processes in PD. (Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Parkinsons disease, Immunogenetics, Genetics, Neuroinflammation
host publication
Parkinson’s Disease : Pathogenesis and Clinical Aspects - Pathogenesis and Clinical Aspects
editor
Stoker, Thomas B. and Greenland, Julia C.
pages
27 - 44
publisher
Codon Publications
ISBN
978-0-9944381-6-4
DOI
10.15586/codonpublications.parkinsonsdisease.2018.ch2
language
English
LU publication?
yes
id
031d39d5-4bdb-4fa6-a8d2-69bfb8a80d12
date added to LUP
2019-06-19 10:13:15
date last changed
2019-06-20 13:31:25
@inbook{031d39d5-4bdb-4fa6-a8d2-69bfb8a80d12,
  abstract     = {{Inflammation is a key feature of Parkinson’s disease (PD). In postmortem PD brains, microglial activation and enhanced major histocompatibility class II (MHCII) expression are seen concomitant to the accumulation of alpha-synuclein (α-synuclein) and loss of dopaminergic cells in the substantia nigra. Recent findings showed that α-synuclein epitopes can be presented and recognized by T-cells. PD is not a single disorder; rather, it encompasses a range of clinical, epidemiological, and genetic subtypes. Around 10% of the cases have a monogenic origin, and several of the disease-causing mutations are linked to inflammatory processes. The remaining 90% of the cases are complex, where environmental and genetic risk factors synergize to induce PD pathology. To date, 41 genetic loci have been identified in genome-wide association studies as associated with PD risk, and among these, two are within the HLA region, coding for immune genes including MHCII. Thus, genetic and immune findings indicate that the immune system has a role in the etiology of PD. Experimentally, inflammatory stimuli can cause selective nigral cell loss in preclinical models of PD, and MHCII is required to elicit α-synuclein-induced pathology in mice. In this chapter, we focus on immunogenetics, that is, the relation between genetic risk factors and immune processes in PD.}},
  author       = {{Swanberg, Maria and Jimenez-Ferrer, Itzia}},
  booktitle    = {{Parkinson’s Disease : Pathogenesis and Clinical Aspects}},
  editor       = {{Stoker, Thomas B. and Greenland, Julia C.}},
  isbn         = {{978-0-9944381-6-4}},
  keywords     = {{Parkinsons disease; Immunogenetics; Genetics; Neuroinflammation}},
  language     = {{eng}},
  month        = {{12}},
  pages        = {{27--44}},
  publisher    = {{Codon Publications}},
  title        = {{Immunogenetics of Parkinson's disease}},
  url          = {{http://dx.doi.org/10.15586/codonpublications.parkinsonsdisease.2018.ch2}},
  doi          = {{10.15586/codonpublications.parkinsonsdisease.2018.ch2}},
  year         = {{2018}},
}