Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA 02115, USA.
Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Cell. 2016 Jun 30;166(1):13-5. doi: 10.1016/j.cell.2016.06.034.
Mutations in the presenilins that cause familial Alzheimer's disease alter the activity of these proteases to increase generation of an aggregation-prone isoform of the amyloid β-peptide (Aβ). How these mutations do so has been unclear. Sannerud et al. now show that regulation of subcellular localization plays a central role, advancing our understanding of the cell biology of Alzheimer's disease.
导致家族性阿尔茨海默病的早老素突变会改变这些蛋白酶的活性，从而增加淀粉样β肽（Aβ）的聚集倾向异构体的生成。这些突变是如何发生的还不清楚。Sannerud 等人现在表明，细胞内定位的调节起着核心作用，这提高了我们对阿尔茨海默病细胞生物学的理解。
