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Accelerated Plaque Accumulation, Associative Learning Deficits, and Up-regulation of α7 Nicotinic Receptor Protein in Transgenic Mice Co-expressing Mutant Human Presenilin 1 and Amyloid Precursor Proteins
Open accessAbstract
Familial Alzheimer's disease-associated mutations in presenilin 1 or 2 or amyloid precursor protein result in elevated beta-amyloid, beta-amyloid accumulation, and plaque formation in the brains of affected individuals. By crossing presenilin 1 transgenic mice carrying the A246E mutation with plaque-producing amyloid precursor protein K670N/M671L transgenic mice (Tg2576), we show that co-expression of both mutant transgenes results in acceleration of amyloid accumulation and associative learning deficits. At 5 months of age with no detectable plaque pathology, amyloid precursor protein transgenic animals are impaired in contextual fear learning following two pairings of conditioned and unconditioned stimuli but appear normal following a more robust five-pairing training. At 9 months of age when beta-amyloid deposition is evident, these mice are impaired following both two-pairing and five-pairing protocols. Mice carrying both transgenes are impaired in contextual fear conditioning at either age. All transgenic animal groups performed as well as controls in cued fear conditioning, indicating that the contextual fear learning deficits are hippocampus-specific. The associative learning impairments are coincident with elevated alpha 7 nicotinic acetylcholine receptor protein in the dentate gyrus. These findings provide two robust and rapid assays for beta-amyloid-associated effects that can be performed on young animals: impaired contextual fear learning and up-regulation of alpha 7 nicotinic receptors.
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“Our findings are also consistent with research showing that increasing Ab by expressing FAD mutant PS1 together with FAD mutant APP failed to produce substantial enhancements of the behavioral deficits observed in mice overexpressing FAD mutant APP alone (56)(57)(58).”
From Amyloid precursor protein-induced axonopathies are independent of amyloid-β peptides (2008) · cites this paper as [56]
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“Fear in Tg2576 mice is a common observation made in this genotype (Dineley et al., 2002).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Dineley et al., 2002
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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 [33]
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Cited by
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Aβ Oligomers – a decade of discovery
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BackgroundInfluentialDocosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model
Calon, F., Lim, G. P., Yang, F., Morihara, T., Teter, B., Ubeda, O., Rostaing, P., Triller, A., Salem, N., Ashe, K. H., et al. (2004) · Neuron · doi:10.1016/j.neuron.2004.08.013 · Cited by 707
“α7 nicotinic receptors are putative Aβ42 receptors that are elevated in PS1 × 0215 Tg2576 mice (Dineley et al., 2002) and that can internalize toxic Aβ species (Nagele et al.”
Nicotinic acetylcholine receptors and the regulation of neuronal signalling
Dajas‐Bailador, F., & Wonnacott, S. (2004) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2004.04.006 · Cited by 618
Alzheimer's disease: synaptic dysfunction and Aβ
Shankar, G. M., & Walsh, D. M. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-48 · Cited by 486
“In addition, the same Tg2576 mice demonstrate poor performance in a hippocampus-dependent contextual fear conditioning assay, decreased spine density in the dentate gyrus, and impairment of long term potentiation (LTP) at ages long before the first detection of Aβ dodecamer [86,90,91].”
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“This model is supported by reports that α7* nAChRs are upregulated in several AD patient cell types, including astrocytes and neurons [93–96], as well as in AD animal models [97], and neuronal cell cultures chronically exposed to Aβ [98].”
Self-citationGong, B., Vitolo, O. V., Trinchese, F., Liu, S., Shelanski, M., & Arancio, O. (2004) · Journal of Clinical Investigation · doi:10.1172/jci22831 · Cited by 442
“These findings are also consistent with previous results in other models of AD (24, 25) and indicate that APP/PS1 mice have a selective hippocampus-dependent impairment in associative learning.”
ResultGong, B., Cao, Z., Zheng, P., Vitolo, O. V., Liu, S., Staniszewski, A., Moolman, D. L., Zhang, H., Shelanski, M. L., & Arancio, O. (2006) · Cell · doi:10.1016/j.cell.2006.06.046 · Cited by 425
The role of CREB and BDNF in neurobiology and treatment of Alzheimer's disease
Amidfar, M., de Oliveira, J., Kucharska, E., Budni, J., & Kim, Y. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118020 · Cited by 419
Progressive age‐related development of Alzheimer‐like pathology in APP/PS1 mice
Trinchese, F., Liu, S., Battaglia, F., Walter, S., Mathews, P. M., & Arancio, O. (2004) · Annals of Neurology · doi:10.1002/ana.20101 · Cited by 384
Interactions between β-amyloid and central cholinergic neurons: implications for Alzheimer’s disease
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Mouse models of Alzheimer's disease
Hall, A. M., & Roberson, E. D. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2011.11.017 · Cited by 317
Temporal memory deficits in Alzheimer’s mouse models: Rescue by genetic deletion of BACE1
Ohno, M., Chang, L., Tseng, W., Oakley, H., Citron, M., Klein, W. L., Vassar, R., & Disterhoft, J. F. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2005.04551.x · Cited by 298
“This result is consistent with previous reports showing normal cued fear conditioning in Tg2576 mice (Corcoran et al., 2002; Dineley et al., 2002), and implies that these transgenic mouse models of AD exhibit specific temporal memory deficits without generalized deficits in expressing freezing as a…”
BackgroundResultInfluentialHippocampal neurogenesis: Learning to remember
Lazarov, O., & Hollands, C. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.12.006 · Cited by 297
“Analysis of mouse models of AD, using many forms of patial tasks has demonstrated deficits in spatial learning (Dineley et al., 2002, Westerman et al., 2002, Trinchese et al., 2004, Comery et al., 2005, Jacobsen et al., 2006, Riddell et al., 2007, Saydoff et al., 2013).”
BackgroundFischer, A., Sananbenesi, F., Pang, P. T., Lu, B., & Tsai, L.-H. (2005) · Neuron · doi:10.1016/j.neuron.2005.10.033 · Cited by 277
“Similarly, several mouse models for neurodegenerative diseases display cognitive deficits in learning paradigms such as the Morris water maze test (Ashe, 2001) and fear conditioning (Dineley et al., 2002).”
BackgroundDinkins, M. B., Enasko, J., Hernandez, C. M., Wang, G., Kong, J., Helwa, I., Liu, Y., Terry, A. V., & Bieberich, E. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.1429-16.2016 · Cited by 249
“Fearconditioned associative learning was assessed in male mice and analyzed (double-blinded) as described previously (Dineley et al., 2002).”
MethodPuzzo, D., Vitolo, O. V., Trinchese, F., Jacob, J. P., Palmeri, A., & Arancio, O. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.5291-04.2005 · Cited by 248
β-Amyloid Peptide Activates α7 Nicotinic Acetylcholine Receptors Expressed in Xenopus Oocytes
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Self-citationBehavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines
Puzzo, D., Lee, L. S., Palmeri, A., Calabrese, G., & Arancio, O. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2014.01.011 · Cited by 226
“contextual FC starting at about 3 months, whereas cued FC is normal, indicating that the learning deficits is based upon the hippocampal dysfunction [78,138,140,186].”
BackgroundComery, T. A., Martone, R. L., Aschmies, S., Atchison, K. P., Diamantidis, G., Gong, X., Zhou, H., Kreft, A. F., Pangalos, M. N., Sonnenberg‐Reines, J., et al. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.2693-05.2005 · Cited by 214
“1B) (Corcoran et al., 2002; Dineley et al., 2002).”
BackgroundResultTaglialatela, G., Hogan, D., Zhang, W.-R., & Dineley, K. (2009) · Behavioural Brain Research · doi:10.1016/j.bbr.2008.12.034 · Cited by 217
Self-citationCuadrado‐Tejedor, M., Hervías, I., Ricobaraza, A., Puerta, E., Pérez-Roldán, J., García, C., Franco, R., Aguirre, N., & García‐Osta, A. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01517.x · Cited by 209
“In fact, even though the APP/PS1 mice have an accelerated rate of amyloid deposition, Puzzo et al. (2009) treated them before the onset of Ab accumulation (Dineley et al., 2002), whereas in the present study Tg2576 mice were treated long after the onset of amyloid deposition.”
BackgroundNeuronal nicotinic receptors: A perspective on two decades of drug discovery research
Arneric, S. P., Holladay, M., & Williams, M. (2007) · Biochemical Pharmacology · doi:10.1016/j.bcp.2007.06.033 · Cited by 208
Trinchese, F., Fà, M., Liu, S., Zhang, H., Hidalgo, A., Schmidt, S. D., Yamaguchi, H., Yoshii, N., Mathews, P. M., Nixon, R. A., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci34254 · Cited by 209
Wang, R., Dineley, K. T., Sweatt, J. D., & Zheng, H. (2004) · Neuroscience · doi:10.1016/j.neuroscience.2004.03.048 · Cited by 207
Self-citationHernandez, C. M., Kayed, R., Zheng, H., Sweatt, J. D., & Dineley, K. T. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.5038-09.2010 · Cited by 204
“…evaluated for general health, sensory perceptiveness, activity level, as well as object recognition and associative learning performance at 5 months of age according to our previously published methods (Dineley et al., 2002b, 2007; Taglialatela et al., 2009) with some modifications as described.”
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“(2007) presented some evidence that A 1– 42 binds to membrane lipids but does not bind to the 7nAChR, both increases and decreases in 7nAChR number have been reported in AD animal models and human patients (Bednar et al., 2002; Dineley et al., 2002; Teaktong et al., 2003; Yu et al., 2005; Counts et al., 2007), making…”
BackgroundResearch update: Alpha7 nicotinic acetylcholine receptor mechanisms in Alzheimer's disease
Parri, H. R., Hernandez, C. M., & Dineley, K. T. (2011) · Biochemical Pharmacology · doi:10.1016/j.bcp.2011.06.039 · Cited by 187
Self-citationNeurotrophins, synaptic plasticity and dementia
Arancio, O., & Chao, M. V. (2007) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2007.03.013 · Cited by 156
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“Seemingly contradictory findings about the effects of A on function of nAChRs (Liu et al., 2001; Pettit et al., 2001; Dineley et al., 2002b; Dougherty et al., 2003; Fu and Jhamandas, 2003; Wu et al., 2004a) have been hard to reconcile, although they may be explained by the use of different…”
BackgroundBehavioral phenotypes of amyloid‐based genetically modified mouse models of Alzheimer's disease
Kobayashi, D. T., & Chen, K. S. (2005) · Genes Brain & Behavior · doi:10.1111/j.1601-183x.2005.00124.x · Cited by 182
“…do report spatial memory deficits in Tg2576 mice in the WM as well as other memory tasks sensitive to hippocampal functions such as contextual fear conditioning and Y-maze alternation (Corcoran et al. 2002; Dineley et al. 2002; Kotilinek et al. 2002; Ohno et al. 2004; Westerman et al. 2002).”
BackgroundInfluentialBeyond the Cholinergic Hypothesis: Do Current Drugs Work in Alzheimer's Disease?
Martorana, A., Esposito, Z., & Koch, G. (2010) · CNS Neuroscience & Therapeutics · doi:10.1111/j.1755-5949.2010.00175.x · Cited by 174
Alzheimer disease pathology as a host response
Castellani, R. J., Lee, H.-G., Zhu, X., Perry, G., & Smith, M. A. (2008) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e318177eaf4 · Cited by 171
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“(90), and contextual fear conditioning (91).”
Cole, A. R., Noble, W. J., van Aalten, L., Plattner, F., Meimaridou, R., Hogan, D., Taylor, M., LaFrancois, J. J., Gunn‐Moore, F. J., Verkhratsky, A., et al. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.04829.x · Cited by 169
Self-citationCastillo-Carranza, D. L., Guerrero-Muñoz, M. J., Sengupta, U., Hernandez, C., Barrett, A. D. T., Dineley, K., & Kayed, R. (2015) · The Journal of Neuroscience · doi:10.1523/jneurosci.4989-14.2015 · Cited by 149
“, 1996) provides a model of AD-like pathology, including accumulation of A peptides, plaque deposition, and cognitive deficits that worsen with age (Dineley et al., 2002; Westerman et al., 2002; Hernandez et al., 2010).”
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“Tests concerning contextual memory, such as fear conditioning, is widely used to measure hippocampal functions [5] and can also be applied in AD mouse models [6].”
Ahn, H. J., Hernandez, C. M., Levenson, J. M., Lubin, F. D., Liou, H.-C., & Sweatt, J. D. (2008) · Learning & Memory · doi:10.1101/lm.866408 · Cited by 149
“Thus, like c-rel / mice, CaMKII T286A mutants (Irvine et al. 2005), CREB hypomorphs (Hebda-Bauer et al. 2005), and transgenic Alzheimer’s disease model mice (Dineley et al. 2002) all exhibit long-term memory deficits that can be overcome with additional training.”
BackgroundSelf-citationWebster, S. J., Bachstetter, A. D., & Eldik, L. J. V. (2013) · Alzheimer s Research & Therapy · doi:10.1186/alzrt182 · Cited by 153
Chauhan, N. B. (2006) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2006.05.030 · Cited by 138
Spines, plasticity, and cognition in Alzheimer's model mice
Spires-Jones, T., & Knafo, S. (2012) · Neural Plasticity · doi:10.1155/2012/319836 · Cited by 133
Alzheimer’s disease as oligomeropathy
Ono, K. (2018) · Neurochemistry International · doi:10.1016/j.neuint.2017.08.010 · Cited by 129
“Westerman et al. (2002) and Dineley et al. (2002) reported that memory loss and insoluble Ab aggregates were not connected in APP transgenic mice (Tg2576) and transgenic mice co-expressing mutant presenilin-1 and APP, respectively, which suggested that earlier Ab aggregates disrupted cognition…”
InfluentialBanerjee, P., Samoriski, G., & Gupta, S. (2005) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.104.081976 · Cited by 131
“…A peptides impair hippocampal signaling in an 7 nAChR-dependent manner and are thought to result from increased Ca2 influx and chronic activation of signal transduction cascades (e.g., extracellular signal-regulated kinase 2/mitogen-activated protein kinase) (Dineley et al., 2001, 2002).”
BackgroundFindley, C. A., Bartke, A., Hascup, K. N., & Hascup, E. R. (2019) · ASN NEURO · doi:10.1177/1759091419855541 · Cited by 133
“Regarding differences between Ab40 and Ab42, Ab40 was found to bind with less affinity and decreased potency compared with Ab42 (Wang et al., 2000a; Dineley et al., 2002a).”
InfluentialThakker, D. R., Weatherspoon, M. R., Harrison, J., Keene, T. E., Lane, D. S., Kaemmerer, W. F., Stewart, G. R., & Shafer, L. L. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0813404106 · Cited by 124
“Two days before euthanizing the animals, all mice were assessed for contextual memory by using a fear-conditioning paradigm that reveals a deficit in the Tg2576 mice as early as 9 months of age (32).”
MethodResultInfluentialShankar, G. M., Leissring, M. A., Adame, A., Sun, X., Spooner, E., Masliah, E., Selkoe, D. J., Lemere, C. A., & Walsh, D. M. (2009) · Neurobiology of Disease · doi:10.1016/j.nbd.2009.07.021 · Cited by 126
“…observed well before the first signs of amyloid deposition (Chapman et al., 1999; Hsia et al., 1999; Moechars et al., 1999; Mucke et al., 2000; Dineley et al., 2002; Westerman et al., 2002; Wu et al., 2004) and from studies in which Aβ-mediated deficits of memory were reversed by a single…”
InfluentialInsulin resistance in Alzheimer's disease
Dineley, K. T., Jahrling, J. B., & Denner, L. A. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.09.001 · Cited by 125
Self-citationNewington, J. T., Rappon, T., Albers, S. S., Wong, D. Y. L., Rylett, R. J., & Cumming, R. C. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.366195 · Cited by 115
“Decreased LDHA and PDK1 Expression in tg-AD Mice at 12 Months—The APPswe/PSEN1dE9 double transgenic mouse strain (tg-AD) exhibits pronounced amyloid plaque accumulation and memory deficits at 12 months of age compared with age-matched controls (38, 39).”
BackgroundPlaques, Tangles, and Memory Loss in Mouse Models of Neurodegeneration
Eriksen, J. L., & Janus, C. G. (2007) · Behavior Genetics · doi:10.1007/s10519-006-9118-z · Cited by 146
Corcoran, K. A., Lu, Y., Turner, R. S., & Maren, S. (2002) · Learning & Memory · doi:10.1101/lm.51002 · Cited by 135
“These results replicate and extend a recent report that also shows contextual fear-conditioning deficits in old Tg2576 mice (Dineley et al. 2002).”
BackgroundResultInfluentialCognitive Enhancement with Rosiglitazone Links the Hippocampal PPARγ and ERK MAPK Signaling Pathways
Denner, L. A., Rodriguez-Rivera, J., Haidacher, S. J., Jahrling, J. B., Carmical, J. R., Hernandez, C. M., Zhao, Y., Sadygov, R. G., Starkey, J. M., Spratt, H. M., et al. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.2153-12.2012 · Cited by 112
“Approximately 9 animals per group were subjected to shock threshold test to assess shock sensitivity, as described previously (Dineley et al., 2002).”
MethodResultSelf-citationThe effects of cholesterol on learning and memory
Schreurs, B. G. (2010) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2010.04.010 · Cited by 114
“…and transgenic rodents, indicates it is the oligomeric form of beta amyloid that is important for its toxic effects and its effects on learning and memory (Billings et al., 2005; Billings et al., 2007; Dineley et al., 2002; Lesne et al., 2006; Ma et al., 2007; Morgan, 2003; Shankar et al., 2008).”
BackgroundBeraldo, F. H., Arantes, C., Santos, T. G., Queiroz‐Hazarbassanov, N., Young, K. F., Rylett, R. J., Markus, R. P., Prado, M. A. M., & Martins, V. R. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.157263 · Cited by 106
Pirttimaki, T. M., Codadu, N. K., Awni, A., Pratik, P., Nagel, D. A., Hill, E. J., Dineley, K. T., & Parri, H. R. (2013) · PLoS ONE · doi:10.1371/journal.pone.0081828 · Cited by 103
“reported for this AD model [34,35].”
Self-citationZameer, A., Kasturirangan, S., Emadi, S., Nimmagadda, S. V., & Sierks, M. R. (2008) · Journal of Molecular Biology · doi:10.1016/j.jmb.2008.09.068 · Cited by 96
Quadratic trajectories of brain myelin content: unifying construct for neuropsychiatric disorders
Bartzokis, G. (2003) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.08.001 · Cited by 97
“Additional evidence supporting this possibility comes from observations that in some transgenic animal models of neurodegenerative diseases, the cognitive declines precede the appearance of NP and NFT and correlate instead with markers of myelin damage[43,114].”
BackgroundNicotinic acetylcholine receptors in neurological and psychiatric diseases
Terry, A. V., Jones, K., & Bertrand, D. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106764 · Cited by 90
Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis
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Self-citationAge‐related deterioration of motor function in male and female 5xFAD mice from 3 to 16 months of age
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“Axonal and motor pathology in APP transgenic mouse models Most studies evaluating motor performance in amyloid precursor protein (APP) transgenic mice by using the rotarod or other tasks did not report major abnormalities (Bellucci et al. 2006; Dineley et al. 2002; Lalonde et al. 2002, 2005).”
BackgroundLee, J., Lau, K., Perkinton, M. S., Standen, C. L., Shemilt, S. J. A., Mercken, L., Cooper, J. D., McLoughlin, D. M., & Miller, C. C. J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300503200 · Cited by 83
Allosteric Modulators of the α7 Nicotinic Acetylcholine Receptor
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“Aβ and α7-nAChR are both detected in hippocampus in AD patients and amyloid precursor protein (APP) transgenic mice [55-59], accompanied with prevalent loss of hippocampal neurons [60].”
BackgroundNetwork dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?
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“We employed delay FC paradigm, which proved to be sensitive paradigm used previously to detect progressive memory decline in APP CRND8 mice [25], and to demonstrate memory decline in Tg2576 mice at ages preceding Aβ aggregation and plaque deposition [26].”
Amelioration of early cognitive deficits by aged garlic extract in Alzheimer's transgenic mice
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BackgroundInfluentialAge-progressing cognitive impairments and neuropathology in transgenic CRND8 mice
Hyde, L. A., Kazdoba, T. M., Grilli, M., Lozza, G., Brussa, R., Zhang, Q., Wong, G. T., McCool, M. F., Zhang, L., Parker, E. M., et al. (2005) · Behavioural Brain Research · doi:10.1016/j.bbr.2004.12.017 · Cited by 83
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“The 6E10 antibody recognizes amino acid residues 1–16 in various abnormally processed isoforms of intra- and extracellular human Aβ [11-15], as well as amyloid precursors.”
BackgroundAlterations in Glucose Metabolism on Cognition: A Possible Link Between Diabetes and Dementia
González-Reyes, R. E., Aliev, G., Ávila-Rodriguez, M., & Barreto, G. E. (2016) · Current Pharmaceutical Design · doi:10.2174/1381612822666151209152013 · Cited by 78
Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease
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“In contrary Tg2567 mice did not show any impairment in the rotarod (Dineley et al., 2002; King and Arendash, 2002), but the balance beam test was able to detect deficits (King and Arendash, 2002).”
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Wild-type Presenilin 1 Protects against Alzheimer Disease Mutation-induced Amyloid Pathology
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Self-citationAmyloid precursor protein-induced axonopathies are independent of amyloid-β peptides
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Sphingolipid-Enriched Extracellular Vesicles and Alzheimer’s Disease: A Decade of Research
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“Aβ and α7-nAChR are both detected in hippocampus in AD patients and amyloid precursor protein (APP) transgenic mice [55-59], accompanied with prevalent loss of hippocampal neurons [60].”
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“…pathogenic factor in Alzheimer’s disease (Dodart et al., 2002; Selkoe, 2002; Walsh et al., 2002), as behavioral deficits precede Ab plaque formation in mice genetically engineered to overexpress the human form of the disease (Dineley et al., 2002; Holcomb et al., 1999; Westerman et al., 2002).”
BackgroundAPP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD)
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“N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript Mouse name Activity References APP/C104 normal Nalbantoglu et al., 1997 APP/C100-Flag normal Berger-Sweeney et al., 1999 APP/C100/IND ↑ Boon et al., 2010 APP/C100/WT ↑ Boon et al., 2010 APP/C99 ↓ Lalonde et al., 2002a APP695SWE+PS1/M14…”
BackgroundInfluentialNicotinic Cholinergic Mechanisms in Alzheimer's Disease.
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“…mouse models of AD expressing mutant human APP, sometimes together with mutant presenilins, have been widely used for investigating the AD pathophysiology and to establish new therapeutic strategies (Ashe and Zahs, 2010; Puzzo et al., 2015; Drummond and Wisniewski, 2017; Sasaguri et al., 2017).”
BackgroundNeurologic and motor dysfunctions in APP transgenic mice
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“, 1998), yielding A β plaques with earlier onset than the single transgenic (Dineley et al., 2002).”
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Self-citationAnderson, D. J., Bunnelle, W. H., Surber, B. W., Du, J. Y., Surowy, C. S., Tribollet, E., Marguerat, A., Bertrand, D., & Gopalakrishnan, M. (2007) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.107.130062 · Cited by 52
“For example, 7 nAChR genetic knockout mice have shown impaired performance in ethanol-induced contextual fear conditioning (Wehner et al., 2004) and showed further deterioration in hippocampus-selective associative learning and memory when crossed with Tg2576 animals ( Dineley et al., 2002 ).”
BackgroundDumont, M., Strazielle, C., Staufenbiel, M., & Lalonde, R. (2004) · Brain Research · doi:10.1016/j.brainres.2004.07.052 · Cited by 55
Morley, B. J., & Mervis, R. F. (2012) · Neuroscience · doi:10.1016/j.neuroscience.2012.12.025 · Cited by 51
“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).”
Metadata
- Authors
- Dineley, K. T., Xia, X., Bui, D., Sweatt, J. D., & Zheng, H.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Dineley, Kelly T.
- Sweatt, J. David
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-06
- Volume
- 277
- Issue
- 25
- Pages
- 22768-22780
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1999234381
- Cited by
- 212
- References
- 38
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 6 · 2019: 9 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 8 · 2014: 10 · 2013: 7 · 2012: 15
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health
- National Institute on Aging
- National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- familial Alzheimer's disease, presenilin 1, amyloid precursor protein, Tg2576 mice, amyloid-beta deposition, amyloid plaques, contextual fear conditioning, alpha7 nicotinic acetylcholine receptor, dentate gyrus, hippocampus, transgenic mice
- MeSH terms
- Age Factors, Animals, Behavior, Animal, Fear, Hippocampus, Immunohistochemistry, Learning, Membrane Proteins, Mice, Transgenic, Mutation, Protein Binding, Receptors, Nicotinic, Shock, Time Factors, Immunoblotting, Up-Regulation, Amyloid beta-Protein Precursor, Transgenes, Mice, Presenilin-1, alpha7 Nicotinic Acetylcholine Receptor
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