Quote:
Originally Posted by olsen
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 |
I would think another option would be to find out why/what causes the alphasynuclein to "pathologically morph" in the first place. How is it different from the alphasyn in people without PD? At what point does it begin to morph? There are a lot of questions that could be asked that might get to the actual heart of the matter, in addition to trying to stop it from spreading once it has already morphed.