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Alzheimer's disease

Attack on amyloid-β protein

Nature volume 537, pages 36–37 (2016)Cite this article

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An antibody therapy markedly reduces aggregates of amyloid-β, the hallmark protein of Alzheimer's disease, and might slow cognitive decline in patients. Confirmation of a cognitive benefit would be a game-changer. See Article p.50

It is 25 years1 since the amyloid-β (Aβ) protein was proposed as the trigger for a cascade of events in the brain that lead to Alzheimer's disease. A growing number of anti-Aβ treatments have been developed to short-circuit this cascade — and several are currently being evaluated in people who have already developed or are at risk of developing symptoms of Alzheimer's (www.alzforum.org/therapeutics). On page 50, Sevigny et al.2 report findings from an initial 12-month, placebo-controlled trial of the antibody aducanumab, which selectively binds to potentially harmful soluble and insoluble Aβ aggregates, respectively called Aβ oligomers and fibrils.

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Figure 1: The amyloid hypothesis.

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References

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Authors and Affiliations

  1. Eric M. Reiman is at the Banner Alzheimer's Institute, Phoenix, Arizona 85006 USA.,

    Eric M. Reiman

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  1. Eric M. Reiman
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Correspondence to Eric M. Reiman.

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Competing interests

E.M.R. is a principal investigator of the Alzheimer’s Prevention Initiative (API), which is involved in the evaluation of anti-Aβ and other promising Alzheimer’s prevention therapies.

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Reiman, E. Attack on amyloid-β protein. Nature 537, 36–37 (2016). https://doi.org/10.1038/537036a

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