PerspectiveBiochemistry

The molecular basis of Alzheimer's plaques

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Science  06 Oct 2017:
Vol. 358, Issue 6359, pp. 45-46
DOI: 10.1126/science.aap8002

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Summary

The leading cause of dementia in adults is Alzheimer's disease (AD), which accounts for more than 80% of dementia cases worldwide (1). This progressive neurodegenerative disorder is defined by the accumulation of toxic senile amyloid plaques and neurofibrillary tangles in the brain, accompanied by synapse and neuron loss (2). The deposits are composed of misfolded protein aggregates, which can also be seeded in a prion-like manner (3); AD is therefore commonly characterized as a protein-misfolding disease. Treatment is limited to the deceleration of progression and symptomatic relief (1). On page 116 of this issue, Gremer et al. (4) present a near-atomic resolution structure of amyloid Aβ(1–42) fibrils, which are the main components of amyloid plaques found in AD brains (see the figure). The structure may help to elucidate the mechanism of plaque formation and facilitate finding a cure for the disease.