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Loss of α7 Nicotinic Receptors Enhances β-Amyloid Oligomer Accumulation, Exacerbating Early-Stage Cognitive Decline and Septohippocampal Pathology in a Mouse Model of Alzheimer's Disease
Open accessAbstract
Early Alzheimer's disease (AD) is marked by cholinergic hypofunction, neuronal marker loss, and decreased nicotinic acetylcholine receptor (nAChR) density from the cortex and hippocampus. α7 nAChRs expressed on cholinergic projection neurons and target regions have been implicated in neuroprotection against β-amyloid (Aβ) toxicity and maintenance of the septohippocampal phenotype. We tested the role that α7 nAChRs perform in the etiology of early AD by genetically deleting the α7 nAChR subunit from the Tg2576 mouse model for AD and assessing animals for cognitive function and septohippocampal integrity. Thus, Tg2576 mice transgenic for mutant human amyloid precursor protein (APP) were crossed with α7 nAChR knock-out mice (A7KO) to render an animal with elevated Aβ in the absence of α7 nAChRs (A7KO–APP). We found that learning and memory deficits seen in 5-month-old APP mice are more severe in the A7KO–APP animals. Analyses of animals in early-stage preplaque cognitive decline revealed signs of neurodegeneration in A7KO–APP hippocampus as well as loss of cholinergic functionality in the basal forebrain and hippocampus. These changes occurred concomitant with the appearance of a dodecameric oligomer of Aβ that was absent from all other genotypic groups, generating the hypothesis that increased soluble oligomeric Aβ may underlie additional impairment of A7KO–APP cognitive function. Thus, α7 nAChRs in a mouse model for early-stage AD appear to serve a neuroprotective role through maintenance of the septohippocampal cholinergic phenotype and preservation of hippocampal integrity possibly through influences on Aβ accumulation and oligomerization.
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“Tg2576 mice exhibit elevated Aβ from 2 months old onward, plaques after 6 months old, and cognitive deficits beginning at 5 months old [32,33,34].”
From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [34]
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“…of the holoprotein (CTF- ) are reduced in hippocampus Many lines of evidence suggest a role for soluble oligomeric A species in the pathology of AD (Walsh et al., 2002; Lesné et al., 2006; Kayed et al., 2007; Lacor et al., 2007; Venkitaramani et al., 2007; Glabe, 2008; Poling et al., 2008).”
BackgroundSelf-citationRetractedThe mouse brain in stereotaxic coordinates
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BackgroundCorrelative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
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“…the observed loss of basal ERK activity in A7KO–APP hippocampus may contribute to one or all of the following observations in these mice: learning and memory deficits, loss of cholinergic functionality, and hippocampal neurodegeneration (Sweatt, 2001; Thatcher et al., 2006; Williams et al., 2007).”
BackgroundSelf-citationThe MAPK cascade is required for mammalian associative learning
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BackgroundInfluential
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“In A7KO-APP AD transgenic mice, the absence of alpha-7 nAChRs leads to Aβ accumulation and oligomerization, exacerbating early-stage cognitive decline and septohippocampal pathology (Hernandez et al., 2010).”
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The nicotinic acetylcholine receptor: smoking and alzheimer's disease revisited
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“Nicotine has been shown to be neuroprotective against NMDA-induced excitotoxicity and that nAChR stimulation protected neurons from rotenone-induced, 6-OHDAinduced and beta-amyloid-induced toxicity (57), (33), (120), (13), (20), (2), (41).”
InfluentialEnhancement of nicotinic receptors alleviates cytotoxicity in neurological disease models
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“Recently, Hernandez and colleagues reported that loss of a7 nAChR enhances Ab oligomer accumulation, exacerbating early-stage cognitive decline in transgenic mouse model of AD, the Tg2576, overexpressing a mutated form of APP (‘Swedish’ mutation) [Hernandez et al. 2010].”
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Neuronal and Glial α7 Nicotinic Acetylcholine Receptors: Role in Alzheimer’s Disease Pathophysiology
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“Furthermore, α 7 knockout exacerbated cognitive deficits in pre-plaque-depositing Tg2576 mice and led to increased soluble oligomeric A β , as well as enhanced neuron loss in the hippocampus [301].”
RETRACTED ARTICLE: nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
D'Angelo, C., Costantini, E., Salvador, N., Marchioni, M., Nicola, M. D., Greig, N., & Reale, M. (2021) · Scientific Reports · doi:10.1038/s41598-021-89139-x · Cited by 14
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“However, recent studies have shown that soluble Aβ is an important source of neurotoxicity and is more toxic than fibrous Aβ (Hernandez et al., 2010).”
BackgroundRetinal changes in the Tg-SwDI mouse model of Alzheimer’s disease
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“In early AD, there is impairment in hippocampus-based episodic memory that is improved through enhancement of cholinergic transmission (Hernandez et al., 2010).”
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“…of the disease (Albuquerque et al., 2009; DeKosky et al., 2002; Dineley et al., 2001; Frölich, 2002; Nordberg, 2001; Small and Fodero, 2002), and these changes have been suggested to be homeostatically related (Hahm et al., 2018; Hernandez et al., 2010; Pratt et al., 2011; Small, 2004, 2007).”
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Aβ dimers induce behavioral and neurochemical deficits of relevance to early Alzheimer's disease
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Proteomic Investigation of Murine Neuronal α7-Nicotinic Acetylcholine Receptor Interacting Proteins
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“Interestingly, knock-out mice that cannot express a7 nAChR exhibit increased levels of Ab1–42 in their brains, a phenomenon that might be related to their severely compromised cognitive status [32].”
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“It is thus suggested that α7 receptors could have a protective role, at least in the disease’s beginning [71].”
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CERAMIDE-ENRICHED EXTRACELLULAR VESICLES
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“Moreover, Aβ interacts with the cholinergic receptor α7 nAChR, and promotes NMDA receptors endocytosis and subsequently disrupts cholinergic neurotransmission [54-57].”
BackgroundMelatoninergic Pathways in Alzheimer's Disease
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“Nicotine has been shown to resolve amyloidosis in experimental models of AD [31-32].”
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“groups (Hernandez et al., 2010).”
Self-citationLi, J., Liu, G.-L., Wang, X.-T., Song, Z., Chen, H., Hou, H.-W., & Hu, Q.-Y. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1929468
“Furthermore, various studies on AD model mice have demonstrated that the knockout of the α 7 nAChR gene can have opposing effects, either ameliorating or exacerbating AD pathology (Dziewczapolski et al., 2009; Hernandez et al., 2010).”
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“…acetylcholine release is of interest considering that acetylcholine signaling through the α 7 nicotinic receptor is neurotrophic and metabotropic [39–43]. α β This receptor has a much higher EC50 compared to 4 2 [44] which is also involved in maintaining arousal states [4] and competes with the…”
Kumro, J., Tripathi, A., Terry, A. V., Pillai, A., & Blake, D. T. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.03.01.582932
“This notion is further supported by studies which showed loss of α 7 receptors enhances amyloid-beta accumulation and cognitive decline in mice (Hernandez et al., 2010) as well as its reported protective role in AD (M. Hernandez & T. Dineley, 2012).”
BackgroundResultBruszt, N., Bali, Z. K., Nagy, L. V., Bodó, K., Engelmann, P., Ledneczki, I., Némethy, Z., Lendvai, B., & Hernádi, I. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.09.20.558650
“Several studies found that expression of α7 nAChRs markedly decreased in NCDs, mainly in brain areas related to cognitive functions such as the frontal cortex and hippocampus (Burghaus et al. 2000; Wevers et al. 2000; Hernandez et al. 2010; Ren et al. 2020).”
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“The oligomers have a number of neurobiological targets, and prominent among them are α7 nicotinic acetylcholine receptors(Caterina M. Hernandez et al., 2010; Inestrosa et al., 2013; Lilja et al., 2011; Sadigh-Eteghad et al., 2014).”
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Modeling ion permeation in wild-type and mutant human α7 nachr ion channels
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“Measurement of shock threshold The shock thresholds for flinching, jumping, and vocalization, which are used as indices of sensitivity to a shock stimulus, were measured as previously described (Hernandez et al., 2010).”
MethodSelf-citationFaucher, P. (2015) · theses.fr (ABES) · doi:10.70675/32388e8eze91bz48c8z8d7fzbc873b067cfd
“A l’inverse, une seconde étude menée sur des souris APP-α7KO âgées de 5 mois, a montré que l’absence des α7-nAChRs potentialisait les déficits mnésiques observés en conditionnement contextuel et en reconnaissance d’objet, et augmentait les niveaux d’Aβ au niveau hippocampique (Hernandez et al., 2010).”
BackgroundInfluential
Metadata
- Authors
- Hernandez, C. M., Kayed, R., Zheng, H., Sweatt, J. D., & Dineley, K. T.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Baylor College of Medicine (US)
- University of Alabama at Birmingham (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-02-17
- Volume
- 30
- Issue
- 7
- Pages
- 2442-2453
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2947456
- OpenAlex
- W1982706802
- Cited by
- 204
- References
- 92
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 12 · 2023: 13 · 2022: 4 · 2021: 9 · 2020: 9 · 2019: 9 · 2018: 15 · 2017: 7 · 2016: 15 · 2015: 19 · 2014: 11 · 2013: 18 · 2012: 18
- FWCI
- 13.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- American Health Assistance Foundation
- McKnight Foundation
- American Psychological Association
- National Institutes of Health
- National Institute on Aging (R01-AG20670, R01AG033467, R01AG020670, R01AG031722)
- National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke (R01NS40039, R01NS013546, R01NS040039)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- alpha7 nicotinic acetylcholine receptor, amyloid-beta oligomers, Alzheimer's disease, Tg2576 mice, amyloid precursor protein, cognitive decline, septohippocampal cholinergic system, hippocampal neurodegeneration, cholinergic hypofunction, learning and memory impairment, neuroprotection
- MeSH terms
- Alzheimer Disease, Analysis of Variance, Animals, Behavior, Animal, Cell Count, Choline O-Acetyltransferase, Cognition Disorders, Conditioning, Classical, Disease Models, Animal, Exploratory Behavior, Fear, Hippocampus, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Neural Pathways, Neurons, Pattern Recognition, Visual, Peptide Fragments, Receptors, Nicotinic, Retention, Psychology, Time Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Septum of Brain, Immunoprecipitation, Mice, NFI Transcription Factors, alpha7 Nicotinic Acetylcholine Receptor
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