Hippocampal Injections of Oligomeric Amyloid β-peptide (1–42) Induce Selective Working Memory Deficits and Long-lasting Alterations of ERK Signaling Pathway
Open accessAbstract
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 their long-lasting impacts on molecular and cognitive functions. In addition, the injections have been most often performed in ventricles, but not in the hippocampus, in spite of the fact that the hippocampus is importantly involved in memory processes and is strongly and precociously affected during the early stages of AD. Thus, in the present study, we investigated the long-lasting impacts of intra-hippocampal injections of oligomeric forms of Aβo(1-42) on working and spatial memory and on the related activation of ERK1/2. Indeed, the extracellular signal-regulated kinase (ERK) which is involved in memory function had been found to be activated by amyloid peptides. We found that repeated bilateral injections (1injection/day over 4 successive days) of oligomeric forms of Aβo(1-42) into the dorsal hippocampus lead to long-lasting impairments in two working memory tasks, these deficits being observed 7 days after the last injection, while spatial memory remained unaffected. Moreover, the working memory deficits were correlated with sustained impairments of ERK1/2 activation in the medial prefrontal cortex (mPFC) and the septum, two brain areas tightly connected with the hippocampus and involved in working memory. Thus, our study is first to evidence that sub-chronic injections of oligomeric forms of Aβo(1-42) into the dorsal hippocampus produces the main sign of cognitive impairments corresponding to the early stages of AD, via long-lasting alterations of an ERK/MAPK pathway in an interconnected brain networks.
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Intra-hippocampal injections of Aβ oligomers cause memory loss correlated with ERK1/2 pathway activation.
“Similarly, intra-hippocampal injections of Aβ oligomers showed loss of memory, correlated with the ERK1/2 pathway activation, which is involved in memory function [145].”
From Alzheimer's Disease: Treatment Strategies and Their Limitations. (2022) · cites this paper as [145]
The Discussion reports that intra-hippocampal Aβ oligomer injections caused working-memory impairments associated with a blockade of test-induced ERK1/2 activation in specific brain structures. The claim captures the link to ERK1/2 signaling but omits the decisive direction: the observed change was impaired activation, not activation associated with memory loss. (LLM, conf=0.86)
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- Authors
- Faucher, P., Mons, N., Micheau, J., Louis, C., & Beracochea, D. J.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Institut de Recherches Internationales Servier (France) (FR)
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2016-01-11
- Volume
- 7
- Pages
- 245-245
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC4707555
- OpenAlex
- W2238119500
- Cited by
- 100
- References
- 99
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 16 · 2022: 13 · 2021: 11 · 2020: 18 · 2019: 6 · 2018: 10 · 2017: 6 · 2016: 5
- FWCI
- 7.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Centre National de la Recherche Scientifique
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, hippocampus, working memory deficits, spatial memory, ERK signaling, MAPK signaling, medial prefrontal cortex, septum, intracerebral injection, early Alzheimer's disease, cognitive impairment
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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