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

Sorting Out Presenilins in Alzheimer's Disease.

Author information

1
Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA 02115, USA. Electronic address: mswolfe@partners.org.
2
Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. Electronic address: bruce_yankner@hms.harvard.edu.

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.

PMID:
27368096
DOI:
10.1016/j.cell.2016.06.034
[Indexed for MEDLINE]
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