Three key proteins allow immune cells in the brain to clear out a protein called amyloid-β, which is a hallmark of Alzheimer's disease.
The immune cells, called microglia, normally absorb and digest amyloid-β after lipoproteins called APOE and CLU attach to it. Lino Gonzalez and Morgan Sheng of drug firm Genentech in South San Francisco, California, and their colleagues looked for interactions between human proteins, and found that a receptor on microglia called TREM2 binds to APOE and CLU. Mouse microglia lacking Trem2 were less effective at absorbing amyloid–lipoprotein complexes, and digested them more slowly than normal cells did. Microglia taken from people carrying a TREM2 mutation were also less able to take up the complexes.
Mutations in the genes that encode TREM2, APOE and CLU have been linked to Alzheimer's, and so the results show how these different genetic risk factors could be linked.
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How immune cells clear amyloid. Nature 535, 468–469 (2016). https://doi.org/10.1038/535468e
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DOI: https://doi.org/10.1038/535468e
