Beta-amyloid, ...........a suspected culprit in Alzheimer's disease but many amyloid directed trials have failed:-
Steinman’s team questioned whether aβ is a villain at all. This helped them to try an unusual experiment that may pay off in spades—though it may confuse a lot of people along the way.Noticing some aβ in MS lesions, they created a synthetic version of it and gave it systemically to MS-model mice to figure out its purpose there. To his shock, it reversed their paralysis for as long as it was administered. He reported this in Science Translational Medicine in 2012. In 2013, he reported in that same journal that even small, pared down hexa-peptides from aβ—and from other amyloid-forming proteins like Alpha-b crystalline and tau—could reverse paralysis in MS-model mice. Now “we are tackling neuro-inflammation using amyloid hexa-peptides mostly in models of MS, which is a disease of neuro-inflammation,” he told Bioscience Technology. “In that situation, our amyloid structures definitely make mice better. We have also found the absence of such amyloid structures makes mice worse, whether you knock out aβ or Alpha b-crystallin, or tau, or prion. This could be a whole new potential MS therapy.”
Steinman’s team questioned whether aβ is a villain at all. This helped them to try an unusual experiment that may pay off in spades—though it may confuse a lot of people along the way.Noticing some aβ in MS lesions, they created a synthetic version of it and gave it systemically to MS-model mice to figure out its purpose there. To his shock, it reversed their paralysis for as long as it was administered. He reported this in Science Translational Medicine in 2012. In 2013, he reported in that same journal that even small, pared down hexa-peptides from aβ—and from other amyloid-forming proteins like Alpha-b crystalline and tau—could reverse paralysis in MS-model mice. Now “we are tackling neuro-inflammation using amyloid hexa-peptides mostly in models of MS, which is a disease of neuro-inflammation,” he told Bioscience Technology. “In that situation, our amyloid structures definitely make mice better. We have also found the absence of such amyloid structures makes mice worse, whether you knock out aβ or Alpha b-crystallin, or tau, or prion. This could be a whole new potential MS therapy.”
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