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08-21-2012, 11:07 PM | #1 | |||
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Once again, it is looking like Lewy Bodies may not be the bad guy at all. This article isn't about PD but has many parallels and if this is true it could be a watershed in PD research. Usually, in autopsy it would explain why the extent of LB fibrils does not correlate to the clinical severity of PD. In other words, when alpha-synuclein aggregates is it a normal protective reaction of the brain gone amok?
Holding on to faulty protein delays brain degeneration Cells have a backup system to deal with any misfolded proteins – they are destroyed by a bell-shaped enzyme called a proteasome, which pulls the proteins inside itself and breaks them down. The finding goes against the idea that neurodegenerative disorders should be treated by clearing away misfolded proteins, rather than trying to rescue their function. "People normally think that protease isn't working hard enough," says Nico Dantuma at the Karolinska Institute in Stockholm, Sweden, who was not involved in the study. Stanford U is on a hot streak.... Laura |
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"Thanks for this!" says: | anon72219 (08-22-2012) |
08-22-2012, 08:31 AM | #2 | ||
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We have long been skeptical of the misfolded protein as the cause of PD theory...mainly because no one could show whether it was the actual cause, vs. some protective (or unprotective) side effect of something else amiss. I know they are different, but as Alz. trials continued to show reduction of plaques made things WORSE, we believed more strongly that the tangles were not the actual root cause of things....and so with PD. Something else is off, and the tangles/misfolds are just one side effect/symptom of the underlying problem, just like tremors, balance issues, etc. I don't mean to simplify things, just trying to say that like many conditions, PD is a dominoe chain: one thing gets off, and everything down the line is off as well. I fear scientists have been looking at the dominoes too far down the chain, instead of backing up to the original root of the problem. Maybe now that is changing! |
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