looks like your class may have had it right, TL - based on available research at least
Resveratrol exacerbates both autoimmune and viral models of multiple sclerosis (2013)
https://www.sciencedirect.com/science/a ... 4013005270
"...resveratrol treatment significantly exacerbated demyelination and inflammation without neuroprotection in the central nervous system in both models
. Our findings indicate that caution should be exercised in potential therapeutic applications of resveratrol in human inflammatory demyelinating diseases, including multiple sclerosis."
i am not up to speed on the cuprizone model or other models of ms:
Resveratrol Promotes Remyelination in Cuprizone Model of Multiple Sclerosis: Biochemical and Histological Study (2017)
https://link.springer.com/article/10.10 ... 016-9891-5
"Resveratrol effectively enhanced motor coordination and balance, reversed cuprizone-induced demyelination
, improved mitochondrial function, alleviated oxidative stress, and inhibited NF-κB signaling. Interestingly, resveratrol increased Olig1 expression that is positively correlated to active remyelination. The present study may be the first to indicate a pro-remyelinative effect for resveratrol which might represent a potential additive benefit in treating MS."
"The animals were randomly divided into four experimental groups, each containing 20 mice: cuprizone-intoxicated (CI) group received a diet containing 0.7 % (w/w) cuprizone mixed into standard rodent chow for 7 days , followed by 3 weeks on 0.2 % cuprizone diet plus oral gavage of phosphate-buffered saline (PBS) once/day. Resveratrol-treated group (RT) received a diet containing 0.7 % cuprizone for 7 days, followed by 3 weeks on 0.2 % cuprizone diet plus 250 mg/kg resveratrol in PBS by oral gavage once daily ."
related background info (new to me)
Multiple sclerosis: experimental models and reality (2017)
"Toxic models are highly useful to unravel mechanisms of de- and remyelination, but do not reflect other important aspects of MS pathology and pathogenesis. For all these reasons, it is important to select the right experimental model to answer specific questions in MS research. ...
Toxic Models of demyelination and remyelination
(1) Cuprizone Models 
Highly reproducible time course of demyelination and remyelination; well-defined pathophysiological mechanisms of demyelination
Very good models to study basic biology of demyelination and remyelination
Very efficient spontaneous remyelination after cessation of the toxic injury; permanent remyelination failure, as seen in many MS lesions, is only seen in models with prolonged cuprizone intoxication"
Strain differences in cuprizone induced demyelination (2017)
"We demonstrate that exposure to a diet containing 0.2% cuprizone resulted in less severe demyelination in the midline of the corpus callosum over the fornix in CD1 mice than C57BL/6 mice. With continuous cuprizone feeding, demyelination in CD1 mice was not prominent until after 7 weeks"
afaic the jury is still out on this one
if a toxin is causal where human demyelination is concerned, i'd be more inclined to remove the toxin than keep it and add an herbal. my 2c!