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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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“…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).”
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BackgroundInfluential
Research works printed but not linked: 3
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Amyloid Beta: Structure, Biology and Structure-Based Therapeutic Development
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“In an early AD mouse model, a7 nAChRs also provided neuroprotection through the maintenance of the septo-hippocampal cholinergic phenotype, the preservation of hippocampal integrity, and decreasing the Ab accumulation and oligomerization (Hernandez et al., 2010).”
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BackgroundLipid Rafts and Alzheimer’s Disease: Protein-Lipid Interactions and Perturbation of Signaling
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BackgroundSelf-citationA Sensitive Aβ Oligomer Assay Discriminates Alzheimer's and Aged Control Cerebrospinal Fluid
Savage, M. J., Kalinina, J., Wolfe, A. L., Tugusheva, K., Korn, R., Cash-Mason, T., Maxwell, J. W., Hatcher, N. G., Haugabook, S. J., Wu, G., et al. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.1675-13.2014 · Cited by 187
“In model systems, oligomers are more toxic and correlate with cognitive impairments in AD mouse models (Lesné et al., 2006; Cheng et al., 2007; Hernandez et al., 2010), and humans (Tomic et al.”
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Zhao, L. N., Leong, H., Mu, Y., & Chew, L. Y. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms13067303 · Cited by 163
“Nonetheless, the neuroprotective role of nAChRs by counterbalancing the toxicity of Aβ oligomers has been proposed based on experimental observation [109].”
BackgroundResultThe Basal Forebrain Cholinergic Projection System in Mice
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BackgroundA Role for Calcineurin in Alzheimers Disease
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ResultFunctional α7 Nicotinic ACh Receptors on Astrocytes in Rat Hippocampal CA1 Slices
Shen, J., & Yakel, J. L. (2012) · Journal of Molecular Neuroscience · doi:10.1007/s12031-012-9719-3 · Cited by 119
“Guangdong 515041, People’s Republic of China jxshen@stu.edu.cn mouse model decreases (Dziewczapolski et al. 2009) or enhances (Hernandez et al. 2010) cognitive deficits associated with AD.”
BackgroundAlpha7 nicotinic receptors as therapeutic targets for Parkinson’s disease
Quik, M., Zhang, D., McGregor, M., & Bordia, T. (2015) · Biochemical Pharmacology · doi:10.1016/j.bcp.2015.06.014 · Cited by 113
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Mroczko, B., Groblewska, M., Litman-Zawadzka, A., Kornhuber, J., & Lewczuk, P. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19071884 · Cited by 97
Aβ Internalization by Neurons and Glia
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“Recently, it was shown that the loss of α7nAChR in Tg2576 mice (A7KO-APP mice) enhances Aβ oligomer accumulation in the extracellular space and increases early cognitive decline and septohippocampal pathology in young animals [109], but improves cognitive deficits and synaptic pathology in aged A7KO-APP mice [110].”
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“On the other hand, Targeting α7 nAChR has been suggested to reduce microglia activation and enhance the ability to clear the misfolded and aggregated proteins (Hernandez et al., 2010; Takata et al., 2010; Medeiros et al., 2014).”
BackgroundNeuroprotective effect of curcumin on okadaic acid induced memory impairment in mice
Rajasekar, N., Dwivedi, S., Tota, S., Kamat, P. K., Hanif, K., Nath, C., & Shukla, R. (2013) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2013.04.033 · Cited by 85
“Further loss of α7 nicotinic acetylcholine receptors leads to enhanced β-amyloid oligomer accumulation in mouse model of Alzheimer's disease (Hernandez et al., 2010).”
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“…α7 nAChR in the hippocampus results in significant learning and memory impairments (Levin et al., 2002; Fernandes et al., 2006; Nott & Levin, 2006; Young et al., 2007; Levin et al., 2009), and worsens the learning and memory deficits in a mouse model of Alzheimer’s disease (Hernandez et al., 2010).”
BackgroundThe Prion Protein Ligand, Stress-Inducible Phosphoprotein 1, Regulates Amyloid-β Oligomer Toxicity
Ostapchenko, V. G., Beraldo, F. H., Mohammad, A. H., Xie, Y., Hirata, P. H. F., Magalhães, A. C., Lamour, G., Li, H., Maciejewski, A., Belrose, J. C., et al. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.3214-13.2013 · Cited by 87
“Indeed, A actions via 7 nAChRs may also affect hippocampal LTP (Gu and Yakel, 2011), and genetic depletion of 7 nAChRs in an early-stage AD mouse model exacerbated cognitive deficits and septohippocampal pathology (Hernandez et al., 2010).”
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“Tg2576 also do not portray overt neurodegeneration yet Tg2576 exhibit synapse and volume loss in the hippocampus (Hernandez et al., 2010; Irizarry et al., 1997) which is considered one of the best correlates to cognitive impairment of early, and possibly preclinical, AD (Albert et al., 2011;…”
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“However, 7-nAChRmediated effects may critically depend on animal age (and perhaps background), because one recent study (Hernandez et al., 2010), using a mouse model of AD, suggests that deletion of 7 subunits exacerbates learning deficits in young animals and alters the pattern of A accumulation.”
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“This discrepancy is explained by Hernandez et al. (2010) as a difference in the age of the animals used; the α7 nAChR activity appears to be neuroprotective in early Alzheimer’s disease, whereas it may be deleterious in later stages of Alzheimer’s disease (Dziewczapolski et al. 2009; Hernandez et…”
InfluentialChronic 5-HT4 receptor activation decreases Aβ production and deposition in hAPP/PS1 mice
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“Alternatively, several studies showed degeneration of the cholinergic system inoldADmodelmice (Devi andOhno, 2010;Hernandez et al., 2010; Perez et al., 2011), and activation of 5-HT4 receptors is known to increase acetylcholine levels (Consolo et al., 1994; Yamaguchi et al., 1997a; Yamaguchi et…”
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“Several lines of research point to a central role for the a7 nAChR in the etiology of AD (Wang et al., 2000; Dineley et al., 2002; Chen et al., 2006; Counts et al., 2007; Dziewczapolski et al., 2009; Hernandez et al., 2010; Heinzen et al., 2010; also reviewed in Bencherif and Lippiello, 2011).”
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“The activation of α7nAChR attenuates Aβ toxicity by a high affinity interaction with the Aβ peptide and as such retards the oligomerization of Aβ peptides [29].”
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Cholinergic Mechanisms in the Cerebral Cortex
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Burns, L. H., Pei, Z., & Wang, H. (2023) · Drug Development Research · doi:10.1002/ddr.22085 · Cited by 35
“However, conflicting research showed that loss of α7nAChR in an AD mouse model enhanced Aβ oligomer accumulation and exacerbated cognitive decline and septohippocampal pathology (Hernandez et al., 2010).”
Tropea, M. R., Puma, D. D. L., Melone, M., Gulisano, W., Arancio, O., Grassi, C., Conti, F., & Puzzo, D. (2021) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2021.102154 · Cited by 42
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Chaperoning α7 neuronal nicotinic acetylcholine receptors.
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“Further, loss of a7 nicotinic acetylcholine receptors leads to increased b-amyloid oligomer accumulation in mouse model of AD [27].”
BackgroundSadigh‐Eteghad, S., Mahmoudi, J., Babri, S., & Talebi, M. (2015) · Acta Cirúrgica Brasileira · doi:10.1590/s0102-865020150110000003 · Cited by 50
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Li, S., Wu, M., Wang, X., Yuan, L., Yang, D. U., & Qi, J. (2011) · Synapse · doi:10.1002/syn.20951 · Cited by 30
“However, it is also reported that loss of a7 nAChRs enhanced beta-amyloid oligomer accumulation and exacerbated early stage cognitive decline in a mouse model of AD (Hernandez et al., 2010).”
BackgroundDeutsch, S. I., Burket, J. A., Urbano, M. R., & Benson, A. D. (2015) · Biochemical Pharmacology · doi:10.1016/j.bcp.2015.06.005 · Cited by 32
Otto, S. L., & Yakel, J. L. (2018) · Brain Structure and Function · doi:10.1007/s00429-018-1799-6 · Cited by 28
Telencephalon transcriptome analysis of chronically stressed adult zebrafish
Huang, V., Butler, A. A., & Lubin, F. D. (2019) · Scientific Reports · doi:10.1038/s41598-018-37761-7 · Cited by 33
Fawzi, S. F., Menze, E. T., & Tadros, M. G. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.112314 · Cited by 26
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“Tg2576 also do not portray overt neurode-generation yet Tg2576 exhibit synapse and volume loss in the hippocampus [147, 172] which is consid-eredoneofthebestcorrelatestocognitiveimpairmentofearly,andpossiblypreclinical,AD[8,9,44, 173].”
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“demonstrated that memory deficits in neurodegenerative diseases are often characterized by decreased cholinergic terminals in the hippocampus [10,11,23,24,25], which further highlights the role of cholinergic receptors in memory.”
BackgroundCharacterization of the Brain β-Amyloid Isoform Pattern at Different Ages of Tg2576 Mice
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“A loss of α7-nAChR exacerbates early-stage cognitive decline and septohippocampal pathology in a mouse model of AD (Hernandez et al., 2010; Cheng et al., 2015).”
BackgroundBrain Imaging of Nicotinic Receptors in Alzheimer's Disease
Wu, J., Ishikawa, M., Zhang, J., & Hashimoto, K. (2010) · International Journal of Alzheimer s Disease · doi:10.4061/2010/548913 · Cited by 211
“The cognitive deficits seen in APP transgenic mice worsen when α7 nAChR is absent at the same time [84].”
BackgroundResultSzegő, É. M., Csorba, A., Janáky, T., Kékesi, K. A., Ábrahám, I. M., Mórotz, G. M., Penke, B., Palkovits, M., Murvai, Ü., Kellermayer, M. S. Z., et al. (2011) · Neuroendocrinology · doi:10.1159/000321119 · Cited by 24
Moyano, P., Garcia, J., Anadon, M., Lobo, M., García, J., Frejo, M., Sola, E., Pelayo, A., & del Pino, J. (2019) · Food and Chemical Toxicology · doi:10.1016/j.fct.2019.02.012 · Cited by 24
Potential Astrocytic Receptors and Transporters in the Pathogenesis of Alzheimer’s Disease
Zhang, X., Lao, K., Qiu, Z., Rahman, M. S., Zhang, Y., & Gou, X. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-181084 · Cited by 24
Sadigh‐Eteghad, S., Majdi, A., Talebi, M., Mahmoudi, J., & Babri, S. (2015) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2015.02.047 · Cited by 29
Hahm, E.-T., Nagaraja, R. Y., Waro, G., & Tsunoda, S. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.06.029 · Cited by 24
“This homeostatic response has been proposed to initially protect the system from cognitive decline (Hernandez et al., 2010; Pratt et al., 2011; Small, 2004, 2007) but eventually facilitate later neurodegeration (Small, 2004, 2008).”
BackgroundDrug Development in Alzheimer’s Disease: The Contribution of PET and SPECT
Declercq, L., Vandenberghe, R. R., Laere, K. V., Verbruggen, A., & Bormans, G. M. (2016) · Frontiers in Pharmacology · doi:10.3389/fphar.2016.00088 · Cited by 27
“…and tau (3xTg-ADmice) (Oddo et al., 2003; Billings et al., 2005; Kitazawa et al., 2005) were consistent with the aforementioned in vitro conclusions for human AD, demonstrating an age dependent reduction of α7 nAChR, as higher Aβ may eventually block remaining α7 nAChRs (Hernandez et al., 2010).”
Huang, X., Cheng, Z., Su, Q., Zhu, X., Wang, Q., Chen, R., & Wang, X. (2012) · International Journal of Neuroscience · doi:10.3109/00207454.2012.657377 · Cited by 23
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Cao, K., Dong, Y., Xiang, J., Xu, Y., Li, Y., Song, H., Yu, W., Qi, X., & Guan, Z.-Z. (2019) · Aging · doi:10.18632/aging.102713 · Cited by 26
“Other evidence indicates that α7 nAChR is involved in memory and cognitive functions and plays a neuroprotective role in AD by influencing the accumulation and oligomerization of Aβ [54, 55].”
Backgroundα7 nicotinic acetylcholine receptor in memory processing
Pastor, V. E., & Medina, J. H. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.15913 · Cited by 24
“Despite existing evidence about molecular interaction between A β and α 7 nAChRs (Wang et al., 2000), contradictory results have been reported about the contribution of α 7 nAChRs to the pathophysiology of AD (Dziewczapolski et al., 2009; Hernandez et al., 2010).”
BackgroundMa, K., Lv, J., Yang, W., Chang, K.-W., Hu, X., Shi, L., Zhai, W.-Y., Zong, H.-F., & Qian, Y. (2017) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2017.11.006 · Cited by 21
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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