Hippocampal Injections of oligomeric amyloid β-peptide (1-42) induce selective working memory deficits and long-lasting alterations of ERK signaling pathway.

Hippocampal Injections of oligomeric amyloid β-peptide (1-42) induce selective working memory deficits and long-lasting alterations of ERK signaling pathway.

Increasing evidence suggests that abnormal brain accumulation of soluble rather than aggregated amyloid-β1-42 oligomers (Aβo(1-42)) plays a causal role in Alzheimer’s disease (AD). However, as yet, animal’s models of AD based on oligomeric amyloid-β1-42 injections in the brain have not investigated...

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Bibliographic Details
Main Authors: Pierre eFaucher, Nicole eMons, Jacques eMicheau, Caroline eLouis, Daniel Jacques Beracochea
Format: Article
Language:English
Published: Frontiers Media S.A. 2016-01-01
Series:Frontiers in Aging Neuroscience
Subjects:
Alzheimer Disease
Hippocampus
working memory
ERK/MAPK
Aβo(1-42)
Online Access:http://journal.frontiersin.org/Journal/10.3389/fnagi.2015.00245/full

Internet

http://journal.frontiersin.org/Journal/10.3389/fnagi.2015.00245/full

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