Parkinson's disease spreads in brain similar to infection: Austrian researchers
The team led by Gabor Kovacs said they are now able to show how, with the use of a specially-developed antibody, spreading of the disease occurs in the human brain...
The focus ...on the protein Alpha-synuclein that is abundant in the human brain. In patients with Parkinson's disease ... the protein appears in a pathologically-altered state. The study showed how human nerve cells absorbed the pathologically-altered form of the protein and how it was thus transmitted from one cell to the next... Kovacs said blocking the spreading mechanism of the Alpha-synuclein protein could now be targeted as a means of therapy for patients, and additionally the antibody could be used to aid in making diagnoses of both Parkinson's disease and Lewy body dementia. The announcement from the team supports similar claims from Munich-based neuropathologist Armin Giese, who reported similar behaviour with Alzheimer's disease, on Tuesday last week. http://news.xinhuanet.com/english/he..._133663718.htm |
another target could be finding the cause of alteration
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Curcumin is supposed stop this morphing atleast in vitro. |
Read today of Spanish research into alpha-syn, very interesting, about mechanism for passing on protein changes is reproducible using alpha-syn human cells with lab animal subjects. Promptly lost the link:mad: but sure it came from other pd associates.
Girija, thought of you immediately, and that the paper seemed the closest to finding a cause we have seen yet. It was called something like mechanism for PD found. |
Another paper in the same area:
"α-Synuclein Immunotherapy Blocks Uptake and Templated Propagation of Misfolded α-Synuclein and Neurodegeneration" Hien T. Tran, Charlotte Hiu-Yan Chung, Michiyo Iba, Bin Zhang, John Q. Trojanowski, Kelvin C. Luk, Virginia M.Y. Lee Cell, 26 June, 2014 http://www.cell.com/cell-reports/ful...247(14)00427-6 "Misfolded and aggregated disease-specific proteins such as α-syn in Parkinson’s disease (PD) and Aβ and tau in Alzheimer’s disease (AD) are common features of many neurodegenerative diseases (NDs). Self-amplification, propagation, and transmission of these misfolded proteins are hypothesized as major contributing factors to disease onset and progression." Working with mice, they showed that: "α-syn immunotherapy using Syn303 reduced pathologic spread of α-syn aggregates in vivo, ameliorated motor dysfunction mediated by LB pathology, and rescued TH cell loss." John |
Virigina Lee presentation on a-syn and tau
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Certainly something to speculate about and research more. Gary |
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