Research ArticleMultiple Sclerosis

Reversal of Paralysis and Reduced Inflammation from Peripheral Administration of β-Amyloid in TH1 and TH17 Versions of Experimental Autoimmune Encephalomyelitis

Science Translational Medicine  01 Aug 2012:
Vol. 4, Issue 145, pp. 145ra105
DOI: 10.1126/scitranslmed.3004145

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When Being Bad Is Good

β-Amyloid (Aβ) is one of the supervillains of the Alzheimer’s disease (AD) world. Aβ plaques are a hallmark of the disease and are thought to promote neurotoxicity and inflammation. But what happens when you take Aβ out of the context of AD and examine its role in another disease, such as multiple sclerosis (MS)? Grant et al. do just that in a mouse model of MS—experimental autoimmune encephalomyelitis (EAE)—and find that in some situations, Aβ might not be so bad after all.

In four models of EAE that included both preventative and therapeutic ones, the authors found, contrary to their expectations, that treating with Aβ peptides decreased both inflammation and the severity of disease. Conversely, in EAE mice genetically altered to lack amyloid precursor protein, inflammation was more severe and MS-like symptoms were exacerbated. These anti-inflammatory effects of Aβ appear to depend on immune cells because treatment was also successful in models of EAE caused by transplantation of pathogenic T cells. Although more mechanistic and safety studies need to be performed before Aβ is ready for therapeutic prime time, these data highlight the molecule’s potential anti-inflammatory effects in selected contexts. Like some other presumed villains, Aβ might not be unequivocally bad, just misunderstood.