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Journal ArticleDOI

DJ-1 facilitates the interaction between STAT1 and its phosphatase, SHP-1, in brain microglia and astrocytes: A novel anti-inflammatory function of DJ-1

TLDR
It is suggested that DJ-1 may function as a scaffold protein that facilitates SHP-1 interactions with p-STAT1 and STAT1, thereby preventing extensive and prolonged STAT1 activation.
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This article is published in Neurobiology of Disease.The article was published on 2013-12-01. It has received 77 citations till now. The article focuses on the topics: Microglia & Substantia nigra.

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Journal ArticleDOI

Compromised MAPK signaling in human diseases: an update

TL;DR: Recent research on the roles of MAPK signaling pathways in human diseases, with a focus on cancer and neurodegenerative conditions is summarized.
Journal ArticleDOI

Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes.

TL;DR: The roles of inflammatory response in neurodegenerative diseases are discussed, focusing on the contributions of microglia and astrocytes and their relationship, and biomarkers to measure neuro inflammation and studies on therapeutic drugs that can modulate neuroinflammation are discussed.
Journal ArticleDOI

Oxidative stress and Parkinson’s disease

TL;DR: A mini review of the classical pathways involving these mechanisms of neurodegeneration, the biochemical and molecular events that mediate or regulate DA neuronal vulnerability, and the role of PD-related gene products in modulating cellular responses to oxidative stress in the course of the Neurodegenerative process are given.
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The Role of Astrocyte Dysfunction in Parkinson’s Disease Pathogenesis

TL;DR: Recent studies have determined that genes known to have a causative role in the development of PD are expressed inAstrocytes and have important roles in astrocyte function, and their impact on understanding of the pathophysiology of PD is discussed.
Journal ArticleDOI

Microglia and astrocyte dysfunction in parkinson's disease.

TL;DR: The role of microglia and astrocytes dysfunction in relation to PD-linked mutations and their implications in PD pathogenesis are discussed.
References
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Journal ArticleDOI

A simple method for organotypic cultures of nervous tissue

TL;DR: Hippocampal slices prepared from 2-23-day-old neonates were maintained in culture at the interface between air and a culture medium and yielded thin slices which remain 1-4 cell layers thick and are characterized by a well preserved organotypic organization.
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The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease.

TL;DR: The spatiotemporal progression of neuronal loss related to disease duration can be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.
Journal Article

Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies.

TL;DR: Western blot analyses of highly purified LBs from DLB brains showed that full-length as well as partially truncated and insoluble aggregates of alpha-synuclein are deposited in LBs, which strongly implicate alpha- Synuclein in the formation of LBs and the selective degeneration of neurons in sporadic PD and DLB.
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Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen.

TL;DR: The here hypothesized mechanism offers one possible explanation for the sequential and apparently uninterrupted manner in which vulnerable brain regions, subcortical grays and cortical areas become involved in idiopathic Parkinson's disease.
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