β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors:In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

Dineley, Kelly T.; Westerman, Marcus; Bui, Duy; Bell, Karen; Ashe, Karen Hsiao; Sweatt, J. David

doi:10.1523/jneurosci.21-12-04125.2001

Cited by 462Alzheimer's disease research and treatmentsNicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology Research

β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors:In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

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Dineley, Kelly T., Westerman, Marcus, Bui, Duy, Bell, Karen, Ashe, Karen Hsiao, Sweatt, J. David·2001·The Journal of Neuroscience

DOI 10.1523/jneurosci.21-12-04125.2001PMC PMC6762764

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Abstract

Alzheimer's Disease (AD) is the most common of the senile dementias, the prevalence of which is increasing rapidly, with a projected 14 million affected worldwide by 2025. The signal transduction mechanisms that underlie the learning and memory derangements in AD are poorly understood. β-Amyloid (Aβ) peptides are elevated in brain tissue of AD patients and are the principal component of amyloid plaques, a major criterion for postmortem diagnosis of the disease. Using acute and organotypic hippocampal slice preparations, we demonstrate that Aβ peptide 1-42 (Aβ42) couples to the mitogen-activated protein kinase (MAPK) cascade via α7 nicotinic acetylcholine receptors (nAChRs).In vivo elevation of Aβ, such as that exhibited in an animal model for AD, leads to the upregulation of α7 nAChR protein. α7 nAChR upregulation occurs concomitantly with the downregulation of the 42 kDa isoform of extracellular signal-regulated kinase (ERK2) MAPK in hippocampi of aged animals. The phosphorylation state of a transcriptional mediator of long-term potentiation and a downstream target of the ERK MAPK cascade, the cAMP-regulatory element binding (CREB) protein, were affected also. These findings support the model that derangement of hippocampus signal transduction cascades in AD arises as a consequence of increased Aβ burden and chronic activation of the ERK MAPK cascade in an α7 nAChR-dependent manner that eventually leads to the downregulation of ERK2 MAPK and decreased phosphorylation of CREB protein.

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Aβ oligomers bind to α7 nicotinic acetylcholine receptors (α7 nAChRs) and to metabotropic glutamate receptors, in particular mGluR5.
“Aβ binds to α7 nicotinic acetylcholine receptors (α7 nAChRs) and to metabotropic glutamate receptors, in particular mGluR5 [31–33].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [31]

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Authors: Dineley, K. T., Westerman, M., Bui, D., Bell, K., Ashe, K. H., & Sweatt, J. D.
Affiliations: Baylor College of Medicine (US)
University of Minnesota (US)
ORCID: Dineley, Kelly T.
Ashe, Karen Hsiao
Sweatt, J. David
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2001-06-15
Volume: 21
Issue: 12
Pages: 4125-4133
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.21-12-04125.2001
PMC: PMC6762764
OpenAlex: W4297846234
Cited by: 462
References: 62
Citations by year: 2026: 3 · 2025: 6 · 2024: 9 · 2023: 18 · 2022: 23 · 2021: 11 · 2020: 13 · 2019: 12 · 2018: 15 · 2017: 19 · 2016: 19 · 2015: 14 · 2014: 17 · 2013: 17 · 2012: 17
FWCI: 17.88
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
Funders: National Alliance for Research on Schizophrenia and Depression
National Institute on Aging
National Institute of Mental Health
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: amyloid-beta, Alzheimer's disease, alpha7 nicotinic acetylcholine receptor, mitogen-activated protein kinase, ERK2, CREB phosphorylation, hippocampus, signal transduction, amyloid plaques, long-term potentiation, aged animals

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β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors:In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease

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