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Parkinson's disease and α‐synuclein expression

TLDR
The clinical impact of α‐synuclein locus multiplications, and the implications that this has for Parkinson's disease pathogenesis are outlined; potential strategies for disease‐modifying therapies for this currently incurable disorder are discussed.
Abstract
Genetic studies of Parkinson's disease over the last decade or more have revolutionized our understanding of this condition. α-Synuclein was the first gene to be linked to Parkinson's disease, and is arguably the most important: the protein is the principal constituent of Lewy bodies, and variation at its locus is the major genetic risk factor for sporadic disease. Intriguingly, duplications and triplications of the locus, as well as point mutations, cause familial disease. Therefore, subtle alterations of α-synuclein expression can manifest with a dramatic phenotype. We outline the clinical impact of α-synuclein locus multiplications, and the implications that this has for Parkinson's disease pathogenesis. Finally, we discuss potential strategies for disease-modifying therapies for this currently incurable disorder.

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O1-7-4-1Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson's disease

TL;DR: Clinical and genetic information of 5 Japanese patients with Bardet-Biedl syndrome is summarized and it is found that rare liver fibrosis was detected in two patients, while only two patients had renal dysfunction, thought to be a universal symptom.
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Parkinson-associated risk variant in distal enhancer of α-synuclein modulates target gene expression

TL;DR: This work establishes an experimental paradigm to functionally connect genetic variation with disease-relevant phenotypes by combining genome-wide epigenetic information with clustered regularly-interspaced short palindromic repeats (CRISPR)/Cas9 genome editing in human pluripotent stem cells.
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α-Synucleinopathy associated with G51D SNCA mutation: a link between Parkinson's disease and multiple system atrophy?

TL;DR: A British family with young-onset Parkinson’s disease and a G51D SNCA mutation that segregates with the disease and post-mortem brain examination of the proband revealed atrophy affecting frontal and temporal lobes, which could aid in understanding of α-synuclein biology and its impact on disease phenotype.
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MicroRNA-7 targets Nod-like receptor protein 3 inflammasome to modulate neuroinflammation in the pathogenesis of Parkinson’s disease

TL;DR: This study provides a direct link between miR-7 and NLRP3 inflammasome-mediated neuroinflammation in the pathogenesis of PD and demonstrates for the first time that Nlrp3 is a target gene of microRNA-7 (miR- 7).
References
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Journal ArticleDOI

Parkinsonism: Onset, progression, and mortality

TL;DR: Controversy over the effectiveness of therapeutic measures for parkinsonism is due partially to this wide variability and to the paucity of clinical information about the natural history of the syndrome.
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Staging of brain pathology related to sporadic Parkinson’s disease

TL;DR: This study traces the course of the pathology in incidental and symptomatic Parkinson cases proposing a staging procedure based upon the readily recognizable topographical extent of the lesions.
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Mutation in the α-synuclein gene identified in families with Parkinson's disease

TL;DR: A mutation was identified in the α-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype.
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Alpha-synuclein in Lewy bodies.

TL;DR: Strong staining of Lewy bodies from idiopathic Parkinson's disease with antibodies for α-synuclein, a presynaptic protein of unknown function which is mutated in some familial cases of the disease, indicates that the LewY bodies from these two diseases may have identical compositions.
Journal ArticleDOI

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

TL;DR: Mutations in the newly identified gene appear to be responsible for the pathogenesis of Autosomal recessive juvenile parkinsonism, and the protein product is named ‘Parkin’.
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