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The Synucleinopathies: Twenty Years On.

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TLDR
The work, which led to the identification of α-synuclein in Lewy bodies, Lewy neurites and Papp-Lantos bodies, is reviewed as well as what has happened since.
Abstract
In 2017, it is two hundred years since James Parkinson provided the first complete clinical description of the disease named after him, fifty years since the introduction of high-dose D,L-DOPA treatment and twenty years since α-synuclein aggregation came to the fore. In 1998, multiple system atrophy joined Parkinson’s disease and dementia with Lewy bodies as the third major synucleinopathy. Here we review our work, which led to the identification of α-synuclein in Lewy bodies, Lewy neurites and Papp-Lantos bodies, as well as what has happened since. Some of the experiments described were carried out in collaboration with ML Schmidt, VMY Lee and JQ Trojanowski.

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Complement cascade functions during brain development and neurodegeneration.

TL;DR: The complement system, an essential tightly regulated innate immune system, is a key regulator of normal central nervous system development and function, and aberrant complement component expression and activation in the brain may culminate into marked neuroinflammatory response, neurodegenerative processes and cognitive impairment.
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Karyopherin abnormalities in neurodegenerative proteinopathies.

TL;DR: In this paper, the authors identify karyopherin abnormalities in amyotrophic lateral sclerosis, frontotemporal dementia, Alzheimer's disease, and synucleinopathies including Parkinson's disease and dementia with Lewy bodies.
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Heparin induces α-synuclein to form new fibril polymorphs with attenuated neuropathology

TL;DR: In this article , the structure of α-syn fibrils in complex with heparin, a representative glycosaminoglycan (GAG), determined by cryo-electron microscopy (cryo-EM).
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An Update on the Critical Role of α-Synuclein in Parkinson’s Disease and Other Synucleinopathies: from Tissue to Cellular and Molecular Levels

TL;DR: The aggregation of α-synuclein (α-Syn) plays a critical role in the development of Parkinson's disease (PD) and other synucleinopathies.
Journal ArticleDOI

Astrocyte glutamate transporters are increased in an early sporadic model of synucleinopathy.

TL;DR: A new neuroprotective role of astrocytes in an early sporadic model of syn nucleinopathy is described and light is shed on the mechanisms of glutamate transporter regulation for neuroprotection against glutamatergic excitotoxicity in synucleinopathy.
References
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Journal ArticleDOI

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.
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Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis

TL;DR: It is proposed that this chemical selectively damages cells in the substantia nigra in patients who developed marked parkinsonism after using an illicit drug intravenously.
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