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Specks of insight into Alzheimer’s disease

Inflammatory cues trigger microglial cells to release the protein ASC. It emerges that specks of ASC promote a hallmark of Alzheimer’s disease in the brains of mice — aggregation and deposition of amyloid-β protein.
  1. Richard M. Ransohoff

    1. Richard M. Ransohoff is in the Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

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From one perspective, Alzheimer’s disease can be considered to be relatively simple: it requires the formation of aggregated clumps of the protein amyloid-β in the brain, which promote a string of downstream consequences that lead to dementia. But when all contributing factors are taken into account, it is fearsomely complex. For instance, consider the potential role of inflammatory processes. There are many indicators of inflammation in Alzheimer’s disease1: levels of immune molecules are elevated; neuron-supporting cells called glia react strongly to the abnormal tissue environment; and changes arise in the specialized vasculature of the blood–brain barrier. Furthermore, subtle genetic alterations in glia can augment the risk of developing Alzheimer’s disease2. But despite this evidence, details of how inflammation might promote the disease have been evasive1. On page 355, Venegas et al.3 provide evidence that, in mice, an extracellular form of an immune-activation protein promotes amyloid-β aggregation.

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Nature 552, 342-343 (2017)

doi: https://doi.org/10.1038/d41586-017-08668-6

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