Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease

Abstract As stated by the prevailing amyloid cascade hypothesis, Alzheimer's disease (AD) is caused by the aggregation and cerebral deposition of long amyloid‐β peptide (Aβ) species, which are released from a C‐terminal amyloid precursor protein fragment by γ‐secretase. Mutations in its catalyt...

Full description

Saved in:
Bibliographic Details
Main Authors: Benedikt Kretner, Johannes Trambauer, Akio Fukumori, Janina Mielke, Peer‐Hendrik Kuhn, Elisabeth Kremmer, Armin Giese, Stefan F Lichtenthaler, Christian Haass, Thomas Arzberger, Harald Steiner
Format: Article
Language:English
Published: Springer Nature 2016-03-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201505952
Tags: Add Tag
No Tags, Be the first to tag this record!