News
Report Published in the Journal of Parkinson's Disease
January 19, 2012 - The accumulation of α-synuclein, a small, negatively charged protein, in neural cells, is one of the hallmarks of Parkinson’s disease. It has been suggested that oligomeric α-synuclein causes membranes to become permeable, or to form channels on the outer cell membrane. Now, a group of scientists from Sweden has found a way to reliably replicate α-synuclein aggregation on cell membranes to investigate how different forms of α-synuclein interact with membranes under different conditions and to learn if any of the α-synuclein species can penetrate these membranes. Their results are published in the current issue of the Journal of Parkinson’s Disease.
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January 11, 2012 - Evidence Reviewed in Advances in Neuroimmune Biology
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Findings Published in the Journal of Parkinson's Disease
January 10, 2012 - The pathology of Parkinson’s disease is characterized by a loss of dopamine-producing neurons in the pars compacta of the substantia nigra (SN), an area of the brain associated with motor control, along with the development of α-synuclein (αS) protein in the form of Lewy bodies (LB) in the neurons that survive. The spread of LB pathology is thought to progress along with the clinical course of Parkinson’s disease, although recent studies suggest that they are not the toxic cause of cell death. A new study published in The Journal of Parkinson’s Disease finds no support for a primary pathogenic role of LBs, as neither their distribution nor density was associated with the severity of nigral cell loss.
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New Report Published in the Journal of Parkinson's Disease
December 16, 2011 - Parkinson’s disease is marked by the abnormal accumulation of α-synuclein and the early loss of dopamine neurons in the substantia nigra region of the brain. A polymorphism in the promotor of α-synuclein gene known as NACP-Rep1 has been implicated as a risk factor for the disease. Now, researchers have found that different variants of NACP-Rep1 and its interaction with the microtubule-associated protein tau (MAPT) H1 haplotype can influence the speed of clinical deterioration in patients with Parkinson’s disease.
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