An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss.
Mutations in Amyloid-ß Precursor Protein (APP) and BRI2/ITM2b genes cause Familial Alzheimer and Danish Dementias (FAD/FDD), respectively. APP processing by BACE1, which is inhibited by BRI2, yields sAPPß and ß-CTF. ß-CTF is cleaved by gamma-secretase to produce Aß. A knock-in mouse model of FDD, ca...
Saved in:
Main Authors: | Franco Lombino, Fabrizio Biundo, Robert Tamayev, Ottavio Arancio, Luciano D'Adamio |
---|---|
Format: | article |
Language: | EN |
Published: |
Public Library of Science (PLoS)
2013
|
Subjects: | |
Online Access: | https://doaj.org/article/b963b79505004cc4be19909306a1c4c0 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Similar Items
-
APP is cleaved by Bace1 in pre-synaptic vesicles and establishes a pre-synaptic interactome, via its intracellular domain, with molecular complexes that regulate pre-synaptic vesicles functions.
by: Dolores Del Prete, et al.
Published: (2014) -
Role of phosphodiesterase 5 in synaptic plasticity and memory
by: Daniela Puzzo, et al.
Published: (2008) -
Amyloid precursor protein is trafficked and secreted via synaptic vesicles.
by: Teja W Groemer, et al.
Published: (2011) -
Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits
by: Yifan Wu, et al.
Published: (2019) -
Paternal spatial training enhances offspring’s cognitive performance and synaptic plasticity in wild-type but not improve memory deficit in Alzheimer’s mice
by: Shujuan Zhang, et al.
Published: (2017)