scispace - formally typeset
Open AccessJournal Article

[Biochemistry of Parkinson's disease].

T Nagatsu
- 01 May 1988 - 
- Vol. 60, Iss: 5, pp 358-366
About
This article is published in Seikagaku.The article was published on 1988-05-01 and is currently open access. It has received 220 citations till now. The article focuses on the topics: Peptide sequence.

read more

Citations
More filters
Journal ArticleDOI

Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein.

TL;DR: It is shown that α-synuclein is transmitted via endocytosis to neighboring neurons and neuronal precursor cells, forming Lewy-like inclusions, which provide critical insights into the mechanism of pathological progression in PD and other proteinopathies.
Journal ArticleDOI

Ageing and neuronal vulnerability

TL;DR: Emerging evidence on protein interaction networks that monitor and respond to the normal ageing process suggests that successful neural ageing is possible for most people, but also cautions that cures for neurodegenerative disorders are unlikely in the near future.
Journal ArticleDOI

Expanding insights of mitochondrial dysfunction in Parkinson's disease

TL;DR: How DJ1, PINK1 and OMI/HTRA2 fit into and enhance the understanding of the role of mitochondrial dysfunction in Parkinson's disease are reviewed, and how oxidative stress might be a potential unifying factor in the aetiopathogenesis of the disease is considered.
Book ChapterDOI

Etiology and Pathogenesis of Parkinson’s Disease

TL;DR: Genetic factors clearly contribute to the pathogenesis of Parkinson’s disease, and many studies have shed light on their implication in, not only monogenic, but also sporadic forms of PD.
Journal ArticleDOI

Clinical progression in Parkinson disease and the neurobiology of axons.

TL;DR: It is proposed that ongoing degeneration of axons, not cell bodies, is the primary determinant of clinically apparent progression of disease, and that future experimental therapeutics intended to forestall disease progression will benefit from a new focus on the distinct mechanisms of axon degeneration.
References
More filters
Journal ArticleDOI

Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein.

TL;DR: It is shown that α-synuclein is transmitted via endocytosis to neighboring neurons and neuronal precursor cells, forming Lewy-like inclusions, which provide critical insights into the mechanism of pathological progression in PD and other proteinopathies.
Journal ArticleDOI

Expanding insights of mitochondrial dysfunction in Parkinson's disease

TL;DR: How DJ1, PINK1 and OMI/HTRA2 fit into and enhance the understanding of the role of mitochondrial dysfunction in Parkinson's disease are reviewed, and how oxidative stress might be a potential unifying factor in the aetiopathogenesis of the disease is considered.
Book ChapterDOI

Etiology and Pathogenesis of Parkinson’s Disease

TL;DR: Genetic factors clearly contribute to the pathogenesis of Parkinson’s disease, and many studies have shed light on their implication in, not only monogenic, but also sporadic forms of PD.
Journal ArticleDOI

Clinical progression in Parkinson disease and the neurobiology of axons.

TL;DR: It is proposed that ongoing degeneration of axons, not cell bodies, is the primary determinant of clinically apparent progression of disease, and that future experimental therapeutics intended to forestall disease progression will benefit from a new focus on the distinct mechanisms of axon degeneration.
Journal ArticleDOI

Genetic animal models of Parkinson's disease.

TL;DR: The animal models for these genetic causes of PD, including mutations in LRRK2 and alpha-synuclein and mutations in parkin, DJ-1, and PINK1, are discussed, their limitations, and value.