Quote:
Originally Posted by badboy99
Gentelmen see my latest post:
Parkinson’s disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.
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Badboy, I have read reports where, on autopsy of PWP, they did not find any alpha-synyclein clumps, yet the deceased had been dx'd with PD and been taking PD meds for years.....similarly, there are people who were never dx'd with PD who on autopsy, they found the clumps. Can you reconcile this? To me, all this means is that the clumps are not definitive at all, since some PWP don' t have them (but should) and some non-PD people have them (but shouldn't)!
I have not found any research reconciling these conflicting findings.