However in our opinion, the low probability of MS coincidence with another rare disease, together with the animal studies where MS is never a consideration, makes it more likely that these human examples align with an inside-out model (Figure 2), where a primary biochemical derangement of myelin, coupled with an immune predisposition, culminated in a MS-like phenotype
Aging and metabolic reprogramming of adipose-derived stem cells affect molecular mechanisms related to cardiovascular diseases
10.1038/sj.emboj.7600447 EMBO J
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