Dispersed in the brains of Alzheimer’s patients are disk-shaped lesions about 100 µm across. Whether those lesions, or plaques, are a cause or a consequence of Alzheimer’s disease is controversial, but their composition is clear. The plaques are made from fibrous aggregates—amyloid—of protein or their shorter cousins, peptides.

Amyloid also shows up in the neuropathology of Huntington’s, Parkinson’s, and other pernicious diseases. Once sequestered in amyloid, a protein or a peptide can no longer perform its function. Even if amyloid does not directly cause those diseases, it seems at best a useless, dead-end repository of proteinaceous material.

But as a new paper exemplifies, a less malign view of amyloid is emerging. Roland Riek of ETH Zürich and his collaborators in India, Sweden, and the US have demonstrated that our bodies exploit amyloid as a temporary storage medium for a wide range of hormones, including pain-relieving endorphin and appetite-suppressing bombesin. 1...

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