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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-β(1–42) 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-β(1–42) injections in the brain have not investi...
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| Gepubliceerd in: | Front Aging Neurosci |
|---|---|
| Hoofdauteurs: | , , , , |
| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
Frontiers Media S.A.
2016
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| Onderwerpen: | |
| Online toegang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4707555/ https://ncbi.nlm.nih.gov/pubmed/26793098 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3389/fnagi.2015.00245 |
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