113 research outputs found
COX-2 in the neurodegenerative process of Parkinson's disease
No full textThe author thanks Mrs. Birgit Teismann for her help in the preparation of this manuscript. The author wishes also to acknowledge the support of the Wellcome Trust (WT080782MF) and the NHS Endowment fund (06-09). The author declares that he has no conflict of interest.Peer reviewe
Cellular pathology of Parkinson?s disease: astrocytes, microglia and inflammation
No full textParkinson's disease (PD) is a frequent neurological disorder of the basal ganglia, which is characterized by the progressive loss of dopaminergic neurons mainly in the substantia nigra pars compacta (SNpc). Inflammatory processes have been shown to be associated with the pathogenesis of PD. Activated microglia, as well as to a lesser extent reactive astrocytes, are found in the area associated with cell loss, possibly contributing to the inflammatory process by the release of pro-inflammatory prostaglandins or cytokines. Further deleterious factors released by activated microglia or astrocytes are reactive oxygen species. On the other hand, they may mediate neuroprotective properties by the release of trophic factors or the uptake of glutamate. In this review, we will discuss the different aspects of activated glial cells and potential mechanisms that mediate or protect against cell loss in PD
MPP+-induced toxicity in the presence of dopamine is mediated by COX-2 through oxidative stress
No full textPeer reviewe
Receptor for advanced glycation endproducts (RAGE) deficiency protects against MPTP toxicity
No full textCopyright © 2011 Elsevier Inc. All rights reserved.Peer reviewe
Neurochemical, histological and behavioral profiling of the acute, sub-acute and chronic MPTP mouse model of Parkinson’s disease
No full textACKNOWLEDGMENTS We acknowledge the charity body “Tenovus Scotland” for financially supporting the project. A big thanks goes to the Aberdeen medical research facility for the great animal care and support provided during the conduct of MPPTP administration and animal behavioral testing. We also tanks the Wellcome Trust UK for having supported Katie J. Clephan with a summer vacation scholarship.Peer reviewe
An Ideological City: Koolhaas’ Exodus in the Second Ecumene
No full textIn 1968 the Apollo 8 spacecraft became the first manned vehicle to orbit the moon. This mission is perhaps most famous however, for a photograph called Earthrise, taken by astronaut William Anders. Deemed by Life Books as ‘the most influential environmental photograph ever taken (Rowel, 2003, p. 172),’ it is purportedly the first photograph of our globe in-the-round. Earthrise had been preceded, however, by a 1966 black-and-white image taken by the Lunar Orbiter 1 robotic probe. Marking a seminal shift into an era signified by universal globalization, the world’s first view of Earth appropriately originated from beyond its surface. Six years later in 1972 when Rem Koolhaas created his theoretical project, 'Exodus, or the Voluntary Prisoners of Architecture,' he created an architecture against geo-economic forces of globalization. Critical to Exodus is an opposing spatial impenetrability designed to keep people in, while keeping goods, capital, and politics out. Both architecture and city, Exodus ideologically resists a newly emergent globalized world, manifest in an interconnected world-city that Greek architect Constantinos Doxiadis prefigured as 'Ecumenopolis.' Using Peter Sloterdijk's spatial analysis of globalization, I will place Exodus within this economic and historical context – a counter-cultural space at odds with global architecture and cities. As a discordant proposition, however, Koolhaas provides a place in which humans enter into an ontological space: Sloterdijk’s Sphären (Spheres).</jats:p
Mitochondrial dysfunction in Parkinson's disease : pathogenesis and neuroprotection
No full textPeer reviewe
Chelators in the Treatment of Iron Accumulation in Parkinson's Disease
No full textIron is an essential element in the metabolism of all cells. Elevated levels of the metal have been found in the brains of patients of numerous neurodegenerative disorders, including Parkinson's disease (PD). The pathogenesis of PD is largely unknown, although it is thought through studies with experimental models that oxidative stress and dysfunction of brain iron homeostasis, usually a tightly regulated process, play significant roles in the death of dopaminergic neurons. Accumulation of iron is present at affected neurons and associated microglia in the substantia nigra of PD patients. This additional free-iron has the capacity to generate reactive oxygen species, promote the aggregation of α-synuclein protein, and exacerbate or even cause neurodegeneration. There are various treatments aimed at reversing this pathologic increase in iron content, comprising both synthetic and natural iron chelators. These include established drugs, which have been used to treat other disorders related to iron accumulation. This paper will discuss how iron dysregulation occurs and the link between increased iron and oxidative stress in PD, including the mechanism by which these processes lead to cell death, before assessing the current pharmacotherapies aimed at restoring normal iron redox and new chelation strategies undergoing research
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