Ginsenoside Rb1 has anti alpha-synuclein aggregation effects
 

Ardah et al. report [1]:

"Compelling evidence indicates that α-synuclein (α-syn) aggregation plays a central role in the pathogenesis of Parkinson's disease (PD) and other synucleinopathies. Identification of compounds that inhibit or reverse the aggregation process may thus represent a viable therapeutic strategy against PD and related disorders. Ginseng is a well-known medicinal plant that has been used in East Asia for more than two thousand years to treat several conditions. It is now understood that the pharmacological properties of ginseng can be attributed to its biologically active components, the ginsenosides, which in turn have been shown to have neuroprotective properties. We therefore sought to determine for the first time, the potential of the most frequently used and studied ginsenosides, namely Rg1, Rg3 and Rb1, as anti-amyloidogenic agents. The effect of Rg1, Rg3 and Rb1 on α-syn aggregation and toxicity was determined by an array of biophysical, biochemical and cell-culture-based techniques. Among the screened ginsenosides, only Rb1 was shown to be a potent inhibitor of α-syn fibrillation and toxicity. Additionally, Rb1 exhibited a strong ability to disaggregate preformed fibrils and to inhibit the seeded polymerization of α-syn."

Reference:

[1] Neurobiol Dis. 2015 Feb;74:89-101. doi: 10.1016/j.nbd.2014.11.007. Epub 2014 Nov 15.
"Ginsenoside Rb1 inhibits fibrillation and toxicity of alpha-synuclein and disaggregates preformed fibrils."
Ardah MT1, Paleologou KE2, Lv G3, Menon SA1, Abul Khair SB1, Lu JH4, Safieh-Garabedian B5, Al-Hayani AA6, Eliezer D3, Li M7, El-Agnaf OM8.
GINSENOSIDE RB1 INHIBITS FIBRILLATION AND TOXICITY OF ALPHA-SYNUCLEIN AND DISAGGREGATES PREFORMED FIBRILS

John

Inhibition of c-Abl
 

According to some researchers, targeting the toxic forms of alpha-syn is not sufficient. You also need to inhibit c-Abl.

https://www.neurotalk.org/parkinson-...ml#post1235812