I'll also add that rifampicin (different class of antibiotics) has been shown in vitro and in vivo (mice) to stop alpha-synuclien aggregation - see below. It is actually planned for phase II studies for MSA - a similar disease. While the mechanism is proposed more than just an anti-inflammatory response - I am sure that helps.

I think that just like everyone has their own story as to genetic susceptibility and triggering event - everyone responds differently to anti-inflammatories/immune modulators. Some people may respond better to antibiotics, herbs (curcumin, EGCG, skullcap/baicalein, etc), low-dose naltrexone, etc. Of course most of these also have properties other than anti-inflammatories so you never know what mechanism is working but its likely the aggregated effect. Thats why I believe (as others do on the forum) you need to support/attack on multiple levels.

Rifampicin inhibits alpha-synuclein fibrillation and disaggregates fibrils; Chem Biol. 2004 Nov;11(11):1513-21.

Rifampicin reduces alpha-synuclein in a transgenic mouse model of multiple system atrophy.
Neuroreport 2008;19(13):1271-6.


Double-Blind, Randomized Trial of Rifampicin on Neurologic and Autonomic Function in MSA

MSA is a uniformly fatal neurodegenerative disease. Evidence from a mouse model mimicking the MSA synucleinopathy suggests that the antibiotic rifampicin inhibits development of aggregates and may disaggregate them. We propose a double-blind placebo-controlled clinical trial of rifampicin 600 mg qd x 12 months in 100 subjects with relatively early MSA. The primary endpoint is the UMSARS1 scale.