Common Parkinson's hallmark implicated as key mechanisms in non-familial strain

http://www.barchester.com/Media/News/2012/9/common-parkinsons-hallmark-implicated-as-key-mechanisms-in-nonfamilial-strain.htm

http://www.nature.com/ncomms/journal/v3/n9/full/ncomms2032.html

Piecing the story together from the abstract, research has found that the alpha synuclein gene is transcribed to a longer than usual RNA message in sporadic PD (a process stimulated by those cells making dopamine). This transcript leads to higher production of alpha synuclein protein than the cell needs and the excess is toxic to the mitochondria......... What causes sporadic PD cells to make the longer transcript is not yet clear.
well spotted b2b
what worries me is the bit that says 'intercellular dopamine' makes things worse. is the dopamine produced by l-dopa intercellular? it would be a bit of a b*gger if our medication was actually exacerbating the disease??????
Good point,Turnip. The other neurons which might be zapped by L-DOPA by the same process are the serotonin neurons. They use aromatic amino acid decarboxylase to make serotonin. The same enzyme will decarboxylate L-DOPA to dopamine and that might trigger the build up of toxic levels of alpha synuclein in those neurons. Interestingly, a side effect of chronic L-DOPA treatment is "serotonin depletion" which gives rise to anxiety and desperation.........
...its making be anxious and depressed just reading about it.

don't know if this answerable, but was the rna always wrong or could it have been altered since birth? could an outside infection or toxin do that?