阿尔茨海默病中早老素的分类。

Sorting Out Presenilins in Alzheimer's Disease.

机构信息

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.

出版信息

Cell. 2016 Jun 30;166(1):13-5. doi: 10.1016/j.cell.2016.06.034.

DOI:10.1016/j.cell.2016.06.034

PMID:27368096

Abstract

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.

摘要

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。