I really want to transition from research to recovery, but this does look interesting: Exploring the journey of emodin as a potential neuroprotective agent: Novel therapeutic insights with molecular mechanism of action 2022 sciencedirect.com/science/a...
I found Emodin because it inhibits EBV: pdfs.semanticscholar.org/06...
But it seems to do so much more. Just scroll down to "6.2. Parkinson's disease"
Interesting. It seems easy enough to buy the supplement. I might try it - I’ll let you know how I get on.
Interesting read, thanks for posting. It appears also to activate the Nfr2 pathway. Also mentions about liver toxicity, with higher doses so proceed with caution I would say.
thanks for the links... within the first one... scrolling down to 6.2 -- it reads:---------------------------------------
"Oxidative stress and mitochondrial dysfunction were once thought to be the key contributors in PD pathogenesis, but studies have since then established genetic factors to be the primary culprit for the initiation and propagation of the disease."
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i thought genetic factors affected only 10% to 20% of PWP ... what's your opinion?
Good catch. What is odd is that the reference they seem to be using to make the case PD is primarily genetic is from 1994: bmj.com/content/308/6923/281
I am skeptical about that paragraph.
This study says B12 modulates one of the genes that increases risk
ncbi.nlm.nih.gov/pmc/articl...
But not any B12. Looks like I am taking the wrong B12 
"Interestingly, we found that only AdoCbl, but not the other forms of vitamin B12, exhibited inhibition of LRRK2-G2019S autophosphorylation in MEF cells with an IC50 of ~10 µM, similar to that measured in vitro (Fig. 1f–g). We observed a similar inhibition profile for the different forms of vitamin B12 in macrophages derived from the LRRK2-G2019S transgenic mice (Supplementary information, Fig. S2d). The lack of inhibition displayed by CNCbl, HOCbl, or MeCbl is not understood at present, but one possibility is that differences in cellular uptake, localization and metabolism in the cells may affect their efficacy compared to AdoCbl. Because AdoCbl showed the greatest potential for LRRK2 inhibition in cultured cells, we focused our efforts on this physiological form of vitamin B12."
Says it’s found in Japanese Knotweed, I’m taking that at the moment
I searched for Japanese Knotweed and fell down a rabbit hole!
A SCIENCE-BASED PROTOCOL TO SLOW OR STOP PARKINSON’S DISEASE
by Dr. H. Gordon Ainsleigh, D.C. gordonainsleigh.com/Parkins...
He actually has some reasonable things in his protocol, but also says to drink beer or wine every morning through to the afternoon. He seems to do what others do in drawing protocols based on studies.
He also has a protocol for AD and recommend Lithium. That was from 2013, so he was ahead of the curve: DR GORDY’S KEEP-YOUR-WITS PROTOCOL
PREVENTING & TREATING BOTH ALZHEIMERS AND VASCULAR MEMORY LOSS gordonainsleigh.com/Alzheim...
Hmm wouldn’t let me read it, says 404 not found
Odd. You can go to this page and then click on the PD and AD protocols: gordonainsleigh.com/publica...
That one works!
Gigi216, did you find Japanese knotweed to be beneficial for symptoms? I'm asking two years later, assuming that you would know by now. Thank you!
Is this the only literature in emodin/Japanese knotweed? How compelling is this? I would love to hear some opinions. Thanks!
I dropped the ball on this one. Or maybe I was just waiting for more research to come out. There has:
Emodin inhibits HDAC6 mediated NLRP3 signaling and relieves chronic inflammatory pain in mice 2023 - pmc.ncbi.nlm.nih.gov/articl... This was done with injections: "In summary, emodin treatment blocked the HDAC6/NLRP3 inflammasome signaling, suppresses spinal inflammation and alleviates chronic inflammatory pain."
Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review 2024 - pubs.acs.org/doi/10.1021/ac... "Results: Cellular and animal research indicates that emodin exerts robust multimodal neuroprotection in AD. While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects. Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature. Conclusion: Emodin is a potential anti-AD dietary supplement; however, further studies are warrantied to thoroughly understand its target players and mechanisms. Moreover, human clinical data on emodin-mediated amelioration of AD phenotype is largely lacking, and must be addressed in the future. Lastly, the safety of exogenously supplemented emodin must be thoroughly evaluated."
So... Emodin still looks interesting. I don't see any in vivo trials or anecdotal information on taking it orally. That's all I see on this at this time.
Alternative Therapy that MAY act on a root cause of PD.
Hi. Have any of the men out there had to deal with E.D. as a side effect of prescription drugs for Parkinson's? 
Mannitol for Parkinson's disease
