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Here is an interesting article that I have found:

http://multiple-sclerosis-research.blog ... -this.html

BACKGROUND:

Multiple sclerosis (MS) develops exclusively in humans. Non-human primates are resistant against MS, although they are highly susceptible to the MS animal model, experimental autoimmune encephalomyelitis (EAE). Unravelling of the cause(s) underlying this discrepancy is highly relevant as insights might be gained into the elusive event(s) that trigger(s) MS. A well-established difference between the human primate (Homo sapiens) and non-human primates is that humans are unable to synthesize the sialic acid N-glycolylneuraminic acid (Neu5Gc).

VIEWPOINT:

We propose the concept that long-term ingestion by human primates of the foreign Neu5Gc, via red meat consumption, is an ignored environmental risk factor for MS. Conceptually, incorporation of dietary Neu5Gc into vital regions of the central nervous system, such as the blood-brain barrier (BBB) and the axon-myelin unit, creates targets for binding of de novo synthesized heterophilic anti-NeuGc antibodies. Binding of the antibodies can cause BBB leakage and destabilization of the axon-myelin coupling. The ensuing cytodegeneration and release of self-antigens could be a start of the characteristic pathological features of MS.

The meat-scrap hypothesis: small quantities of meat may promote cooperative hunting in wild chimpanzees (Pan troglodytes)
https://link.springer.com/article/10.10 ... 008-0676-3
"The common chimpanzee, Pan troglodytes, is one of the few true omnivores that regularly hunts in groups."

Vitamin B12 nutrition in some primates in captivity
http://www.karger.com/Article/Abstract/155107
"although the rhesus monkey in the wild is predominantly vegetarian, such small items of animal protein as are eaten (eg insects, small animals and eggs) should be sufficient to maintain amounts of the vitamin in the serum comparable to those found in man."

Peripheral neuropathy associated with vitamin‐B12 deficiency in captive monkeys
http://onlinelibrary.wiley.com/doi/10.1 ... 50206/full
"captive rhesus monkeys fed on vegetarian diets eventually become deficient of vitamin b12 and develop neurological defects"

Human and Chimpanzee Gene Expression Differences Replicated in Mice Fed Different Diets
http://journals.plos.org/plosone/articl ... ne.0001504
"... the human diet is markedly different from the diets of closely related primate species ... we analyzed gene expression in laboratory mice fed diets typical of humans and of chimpanzees. The effects of human diets were found to be significantly different from that of a chimpanzee diet in the mouse liver ... 10% of the genes that differ in their expression between humans and chimpanzee livers differed also between the livers of mice fed the human and chimpanzee diets. "

MS is a relatively rare disease in humans affecting only 1 or 2 people per thousand. The age of onset in humans is early to mid 30's for RRMS and maybe ten years later for PPMS. If the age of onset and the prevalence are the same in other primates you would probably have to look at about 500 monkeys in that age bracket to find one with MS. Has anyone done that?

Also you need an MRI to diagnose MS. How many monkeys get MRIs?

A couple of perhaps better questions along this line would be "Why does multiple sclerosis NOT affect certain groups of human primates?" AND "why have these groups of people been put under the microscope?"

i looked up primates life span in the wild to assess what each year of life would mean in human terms, and landed squarely back on the red meat with the first result i clicked
http://www.livescience.com/9769-humans- ... -apes.html

that was technically the second result in the list, the first was this
http://pin.primate.wisc.edu/aboutp/phys/lifespan.html

so, looks like the chimps get 40-53 years depending which species. if we can assume ms tends to show up at a certain life stage vs after a specific number of years, i think for our primate w ms quest we will be sifting thru a pack of 15-20 y-o chimps.

so many primate mris in the full text (EAE tho):

Non-human primate models of multiple sclerosis
http://onlinelibrary.wiley.com/doi/10.1 ... 114.x/full
"Although these experimental therapies were very effective in controlling EAE in rodents, they are only partially effective in MS patients and in some cases even detrimental (77–80). The question therefore arises whether the rodent models are ‘close enough to MS’ to be sufficiently
predictive for the success of a new therapeutic strategy. The observation that MOG-based tolerization completely protects mice against EAE, but induces fatal demyelinating disease in marmosets illustrates how useful a preclinical animal model closer to humans can be (81)"

i'm so used to seeing murine EAE i didn't even know primate EAE was a thing.

jimmylegs wrote:i'm so used to seeing murine EAE i didn't even know primate EAE was a thing.

If I remember correctly, Copaxone was tested in primate EAE.

The reason why it only affects primates is that herpes virinae including in particular EBV have never been fully controlled by the primate's immune system.

Leonard wrote:The reason why it only affects primates is that herpes virinae including in particular EBV have never been fully controlled by the primate's immune system.

This could make sense if EBV chimps developed something similar to MS

Edit: By the way, maybe something similar happens to the marmoset
http://journals.sagepub.com/doi/abs/10. ... 7317690184
http://www.nature.com/cti/journal/v6/n2 ... 0171a.html

Elimination diets might help. For instance you could see what the result is when the mice/primates are fed diets identical to the first, except free of sugar. Sugar has only been available in modern quantities and concentrations for a couple of hundred years, to most if any, humans.

jimmylegs wrote:so many primate mris in the full text (EAE tho):

Non-human primate models of multiple sclerosis
http://onlinelibrary.wiley.com/doi/10.1 ... 114.x/full
"Although these experimental therapies were very effective in controlling EAE in rodents, they are only partially effective in MS patients and in some cases even detrimental (77–80). The question therefore arises whether the rodent models are ‘close enough to MS’ to be sufficiently
predictive for the success of a new therapeutic strategy. The observation that MOG-based tolerization completely protects mice against EAE, but induces fatal demyelinating disease in marmosets illustrates how useful a preclinical animal model closer to humans can be (81)"

i'm so used to seeing murine EAE i didn't even know primate EAE was a thing.

If you enjoy destroying primates, you might like that "model". Very little can model MS, but giving the animals CSF from human MS sufferers is as close to giving the unfortunate beasts MS as it can be.

The use of human CSF might keep a few mad scientists at bay, just because of the cost. EAE is cheap, dangerous, cruel, and should be banned by the FDA.