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Journal articles on the topic 'APP23'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Lefterov, Iliya, Nicholas F. Fitz, Andrea Cronican, Preslav Lefterov, Matthias Staufenbiel та Radosveta Koldamova. "Memory Deficits in APP23/Abca1+/− Mice Correlate with the Level of Aβ Oligomers". ASN Neuro 1, № 2 (2009): AN20090015. http://dx.doi.org/10.1042/an20090015.

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ABCA1, a member of the ATP-binding cassette family of transporters, lipidates ApoE (apolipoprotein A) and is essential for the generation of HDL (high-density lipoprotein)-like particles in the CNS (central nervous system). Lack of Abca1 increases amyloid deposition in several AD (Alzheimer's disease) mouse models. We hypothesized that deletion of only one copy of Abca1 in APP23 (where APP is amyloid precursor protein) AD model mice will aggravate memory deficits in these mice. Using the Morris Water Maze, we demonstrate that 2-year-old Abca1 heterozygous APP23 mice (referred to as APP23/het)

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2

Kokubo, Hideko, Rakez Kayed, Charles G. Glabe, et al. "Amyloid Beta Annular Protofibrils in Cell Processes and Synapses Accumulate with Aging and Alzheimer-Associated Genetic Modification." International Journal of Alzheimer's Disease 2009 (2009): 1–7. http://dx.doi.org/10.4061/2009/689285.

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Amyloidβ(Aβ) annular protofibrils (APFs) have been described where the structure is related to that ofβbarrel pore-forming bacterial toxins and exhibits cellular toxicity. To investigate the relationship of AβAPFs to disease and their ultrastructural localization in brain tissue, we conducted a pre-embedding immunoelectron microscopic study using anti-annular protofibril antiserum. We examined brain tissues of young- and old-aged amyloid precursor protein transgenic mice (APP23), neprilysin knockout APP23 mice, and nontransgenic littermates.αAPF-immunoreactions tended to be found (1) on plasma

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3

Middei, Silvia, Anna Roberto, Nicola Berretta, et al. "Learning discloses abnormal structural and functional plasticity at hippocampal synapses in the APP23 mouse model of Alzheimer's disease." Learning & Memory 17, no. 5 (2010): 236–40. https://doi.org/10.5281/zenodo.14758657.

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B6-Tg/Thy1APP23Sdz (APP23) mutant mice exhibit neurohistological hallmarks of Alzheimer's disease but show intact basal hippocampal neurotransmission and synaptic plasticity. Here, we examine whether spatial learning differently modifies the structural and electrophysiological properties of hippocampal synapses in APP23 and wild-type mice. While no genotypic difference was found in the pseudotrained mice, training elicited a stronger increase in spine density and a more rapid decay of long-term potentiation (LTP) in APP23 mutants. Thus, learning discloses mutation-related abnormalities regardi

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4

Neumeister, Katharina L., and Matthias W. Riepe. "Bupropion and Citalopram in the APP23 Mouse Model of Alzheimer's Disease: A Study in a Dry-Land Maze." International Journal of Alzheimer's Disease 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/673584.

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Background. Incipient Alzheimer's disease is often disguised as depressive disorder. Over the course of AD, depressive symptoms are even more frequent. Hence, treatment with antidepressants is common in AD. It was the goal of the present study to assess whether two common antidepressants with different mechanisms of action affect spatial learning in a transgenic animal model of Alzheimer's disease.Methods. We assessed spatial memory of male wild-type and B6C3-Tg(APPswe,PSEN1dE9)85Dbo (APP23) transgenic animals in a complex dry-land maze. Animals were treated with citalopram (10 mg/kg) and bupr

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5

Giménez-Llort, Lydia, Daniela Marin-Pardo, Paula Marazuela, and Maria del Mar Hernández-Guillamón. "Survival Bias and Crosstalk between Chronological and Behavioral Age: Age- and Genotype-Sensitivity Tests Define Behavioral Signatures in Middle-Aged, Old, and Long-Lived Mice with Normal and AD-Associated Aging." Biomedicines 9, no. 6 (2021): 636. http://dx.doi.org/10.3390/biomedicines9060636.

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New evidence refers to a high degree of heterogeneity in normal but also Alzheimer’s disease (AD) clinical and temporal patterns, increased mortality, and the need to find specific end-of-life prognosticators. This heterogeneity is scarcely explored in very old male AD mice models due to their reduced survival. In the present work, using 915 (432 APP23 and 483 C57BL/6 littermates) mice, we confirmed the better survival curves in male than female APP23 mice and respective wildtypes, providing the chance to characterize behavioral signatures in middle-aged, old, and long-lived male animals. The

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6

Marazuela, Paula, Berta Paez-Montserrat, Anna Bonaterra-Pastra, Montse Solé та Mar Hernández-Guillamon. "Impact of Cerebral Amyloid Angiopathy in Two Transgenic Mouse Models of Cerebral β-Amyloidosis: A Neuropathological Study". International Journal of Molecular Sciences 23, № 9 (2022): 4972. http://dx.doi.org/10.3390/ijms23094972.

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The pathological accumulation of parenchymal and vascular amyloid-beta (Aβ) are the main hallmarks of Alzheimer’s disease (AD) and Cerebral Amyloid Angiopathy (CAA), respectively. Emerging evidence raises an important contribution of vascular dysfunction in AD pathology that could partially explain the failure of anti-Aβ therapies in this field. Transgenic mice models of cerebral β-amyloidosis are essential to a better understanding of the mechanisms underlying amyloid accumulation in the cerebrovasculature and its interactions with neuritic plaque deposition. Here, our main objective was to e

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7

Wilhelmus, Micha M. M., Elisa Tonoli, Clare Coveney, et al. "The Transglutaminase-2 Interactome in the APP23 Mouse Model of Alzheimer’s Disease." Cells 11, no. 3 (2022): 389. http://dx.doi.org/10.3390/cells11030389.

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Amyloid-beta (Aβ) deposition in the brain is closely linked with the development of Alzheimer’s disease (AD). Unfortunately, therapies specifically targeting Aβ deposition have failed to reach their primary clinical endpoints, emphasizing the need to broaden the search strategy for alternative targets/mechanisms. Transglutaminase-2 (TG2) catalyzes post-translational modifications, is present in AD lesions and interacts with AD-associated proteins. However, an unbiased overview of TG2 interactors is lacking in both control and AD brain. Here we aimed to identify these interactors using a crossb

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8

He, Ping, Zhenyu Zhong, Kristina Lindholm та ін. "Deletion of tumor necrosis factor death receptor inhibits amyloid β generation and prevents learning and memory deficits in Alzheimer's mice". Journal of Cell Biology 178, № 5 (2007): 829–41. http://dx.doi.org/10.1083/jcb.200705042.

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The tumor necrosis factor type 1 death receptor (TNFR1) contributes to apoptosis. TNFR1, a subgroup of the TNFR superfamily, contains a cytoplasmic death domain. We recently demonstrated that the TNFR1 cascade is required for amyloid β protein (Aβ)–induced neuronal death. However, the function of TNFR1 in Aβ plaque pathology and amyloid precursor protein (APP) processing in Alzheimer's disease (AD) remains unclear. We report that the deletion of the TNFR1 gene in APP23 transgenic mice (APP23/TNFR1−/−) inhibits Aβ generation and diminishes Aβ plaque formation in the brain. Genetic deletion of T

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9

Van Dam, Debby, Ellen Vloeberghs, Dorothee Abramowski, Matthias Staufenbiel, and Peter Paul De Deyn. "APP23 Mice as a Model of Alzheimer's Disease: An Example of a Transgenic Approach to Modeling a CNS Disorder." CNS Spectrums 10, no. 3 (2005): 207–22. http://dx.doi.org/10.1017/s1092852900010051.

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AbstractAnimal models are considered essential in research ensuing elucidation of human disease processes and subsequently, testing of potential therapeutic strategies. This is especially true for neurodegenerative disorders, in which the first steps in pathogenesis are often not accessible in human patients. Alzheimer's disease is vastly becoming a major medical and socioeconomic problem in our aging society. Valid animal models for this uniquely human condition should exhibit histopathological, biochemical, cognitive, and behavioral alterations observed in Alzheimer's disease patients. Major

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10

Sorgdrager, FJH, CP van Der Ley, M. van Faassen, et al. "The Effect of Tryptophan 2,3-Dioxygenase Inhibition on Kynurenine Metabolism and Cognitive Function in the APP23 Mouse Model of Alzheimer’s Disease." International Journal of Tryptophan Research 13 (January 2020): 117864692097265. http://dx.doi.org/10.1177/1178646920972657.

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Alzheimer’s disease (AD) is associated with progressive endogenous neurotoxicity and hampered inflammatory regulation. The kynurenine (Kyn) pathway, which is controlled by tryptophan 2,3-dioxygenase (TDO), produces neuroactive and anti-inflammatory metabolites. Age-related Kyn pathway activation might contribute to AD pathology in humans, and inhibition of TDO was found to reduce AD-related cellular toxicity and behavioral deficits in animal models. To further explore the effect of aging on the Kyn pathway in the context of AD, we analyzed Kyn metabolite profiles in serum and brain tissue of t

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11

Albani, Diego, Letizia Polito, and Gianluigi Forloni. "P3-034: Environmental enrichment paradigm in APP23." Alzheimer's & Dementia 7 (July 2011): S525. http://dx.doi.org/10.1016/j.jalz.2011.05.1473.

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12

von Arnim, C. A. F., E. Verstege, S. M. Etrich, and M. W. Riepe. "Mechanisms of hypoxic tolerance in presymptomatic APP23 transgenic mice." Mechanisms of Ageing and Development 127, no. 2 (2006): 109–14. http://dx.doi.org/10.1016/j.mad.2005.09.025.

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13

Vloeberghs, Ellen, Debby Van Dam, Katrien Coen, Matthias Staufenbiel, and Peter Paul De Deyn. "Aggressive male APP23 mice modeling behavioral alterations in dementia." Behavioral Neuroscience 120, no. 6 (2006): 1380–83. http://dx.doi.org/10.1037/0735-7044.120.6.1380.

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14

Ippati, Stefania, Yuanyuan Deng, Julia van der Hoven та ін. "Rapid initiation of cell cycle reentry processes protects neurons from amyloid-β toxicity". Proceedings of the National Academy of Sciences 118, № 12 (2021): e2011876118. http://dx.doi.org/10.1073/pnas.2011876118.

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Neurons are postmitotic cells. Reactivation of the cell cycle by neurons has been reported in Alzheimer’s disease (AD) brains and models. This gave rise to the hypothesis that reentering the cell cycle renders neurons vulnerable and thus contributes to AD pathogenesis. Here, we use the fluorescent ubiquitination-based cell cycle indicator (FUCCI) technology to monitor the cell cycle in live neurons. We found transient, self-limited cell cycle reentry activity in naive neurons, suggesting that their postmitotic state is a dynamic process. Furthermore, we observed a diverse response to oligomeri

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15

Vegeto, Elisabetta, Silvia Belcredito, Serena Ghisletti, Clara Meda, Sabrina Etteri, and Adriana Maggi. "The Endogenous Estrogen Status Regulates Microglia Reactivity in Animal Models of Neuroinflammation." Endocrinology 147, no. 5 (2006): 2263–72. http://dx.doi.org/10.1210/en.2005-1330.

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It has been previously demonstrated that 17β-estradiol (E2) inhibits the response of microglia, the resident brain macrophages, to acute injuries in specific brain regions. We here show that the effect of E2 in acute brain inflammation is widespread and that the hormone reduces the expression of inflammatory mediators, such as monocyte chemoattractant protein-1, macrophage inflammatory protein-2, and TNF-α, induced by lipopolysaccharide, demonstrating that microglia are a direct target of estrogen action in brain. Using the APP23 mice, an animal model of Alzheimer’s disease reproducing chronic

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16

Burbach, Guido J. "Amyloid plaque-associated axonal sprouting in aged APP23 transgenic mice." Annals of Anatomy - Anatomischer Anzeiger 187, no. 4 (2005): 357–59. http://dx.doi.org/10.1016/j.aanat.2005.05.004.

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17

Staufenbiel, Matthias, Martina Stalder, Florian Ermini, Christine Sturchler-Pierrat, Mathias Jucker, and Klaus D. Bornemann. "Inflammatory processes in the APP23 mouse model of Alzheimer's disease." Neurobiology of Aging 21 (May 2000): 227. http://dx.doi.org/10.1016/s0197-4580(00)83353-9.

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18

Van Dam, Debby, Rudi D'Hooge, Matthias Staufenbiel, Chris Van Ginneken, Frans Van Meir, and Peter P. De Deyn. "Age-dependent cognitive decline in the APP23 model precedes amyloid deposition." European Journal of Neuroscience 17, no. 2 (2003): 388–96. http://dx.doi.org/10.1046/j.1460-9568.2003.02444.x.

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19

Thal, D. R., J. Steinmetz, I. Kosterin та ін. "Mechanisms of passive vaccination against amyloid β-protein in APP23 mice". Neurology, Psychiatry and Brain Research 20, № 1 (2014): 24–25. http://dx.doi.org/10.1016/j.npbr.2014.01.173.

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20

Bornemann, Klaus D., Karl-Heinz Wiederhold, Chantal Pauli та ін. "Aβ-Induced Inflammatory Processes in Microglia Cells of APP23 Transgenic Mice". American Journal of Pathology 158, № 1 (2001): 63–73. http://dx.doi.org/10.1016/s0002-9440(10)63945-4.

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21

Boncristiano, Sonia, Michael E. Calhoun, Peter H. Kelly, et al. "Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis." Journal of Neuroscience 22, no. 8 (2002): 3234–43. http://dx.doi.org/10.1523/jneurosci.22-08-03234.2002.

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22

Lalonde, R., M. Dumont, M. Staufenbiel, and C. Strazielle. "Neurobehavioral characterization of APP23 transgenic mice with the SHIRPA primary screen." Behavioural Brain Research 157, no. 1 (2005): 91–98. http://dx.doi.org/10.1016/j.bbr.2004.06.020.

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23

Kelly, P. H., L. Bondolfi, D. Hunziker, et al. "Progressive age-related impairment of cognitive behavior in APP23 transgenic mice." Neurobiology of Aging 24, no. 2 (2003): 365–78. http://dx.doi.org/10.1016/s0197-4580(02)00098-2.

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24

Katsouri, Loukia, Yau M. Lim, Katrin Blondrath та ін. "PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase in an Alzheimer’s disease model". Proceedings of the National Academy of Sciences 113, № 43 (2016): 12292–97. http://dx.doi.org/10.1073/pnas.1606171113.

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Current therapies for Alzheimer’s disease (AD) are symptomatic and do not target the underlying Aβ pathology and other important hallmarks including neuronal loss. PPARγ-coactivator-1α (PGC-1α) is a cofactor for transcription factors including the peroxisome proliferator-activated receptor-γ (PPARγ), and it is involved in the regulation of metabolic genes, oxidative phosphorylation, and mitochondrial biogenesis. We previously reported that PGC-1α also regulates the transcription of β-APP cleaving enzyme (BACE1), the main enzyme involved in Aβ generation, and its expression is decreased in AD p

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25

STURCHLER-PIERRAT, CHRISTINE, and MATTHIAS STAUFENBIEL. "Pathogenic Mechanisms of Alzheimer's Disease Analyzed in the APP23 Transgenic Mouse Model." Annals of the New York Academy of Sciences 920, no. 1 (2006): 134–39. http://dx.doi.org/10.1111/j.1749-6632.2000.tb06915.x.

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26

Vloeberghs, Ellen, Debby Van Dam, Rudi D’Hooge, Matthias Staufenbiel, and Peter Paul De Deyn. "APP23 mice display working memory impairment in the plus-shaped water maze." Neuroscience Letters 407, no. 1 (2006): 6–10. http://dx.doi.org/10.1016/j.neulet.2006.07.060.

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27

Vloeberghs, Ellen, Debby Van Dam, Sebastiaan Engelborghs, Guy Nagels, Matthias Staufenbiel, and Peter Paul De Deyn. "Altered circadian locomotor activity in APP23 mice: a model for BPSD disturbances." European Journal of Neuroscience 20, no. 10 (2004): 2757–66. http://dx.doi.org/10.1111/j.1460-9568.2004.03755.x.

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28

Stalder, Martina, Amie Phinney, Alphonse Probst, Bernd Sommer, Matthias Staufenbiel, and Mathias Jucker. "Association of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice." American Journal of Pathology 154, no. 6 (1999): 1673–84. http://dx.doi.org/10.1016/s0002-9440(10)65423-5.

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29

Münch, Christoph, Bing-gen Zhu, Andreas Mink, et al. "Chemical Hypoxia Facilitates Alternative Splicing of EAAT2 in Presymptomatic APP23 Transgenic Mice." Neurochemical Research 33, no. 6 (2007): 1005–10. http://dx.doi.org/10.1007/s11064-007-9540-5.

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30

Laws, Simon M., Patricia Friedrich, Matthias Staufenbiel, Frauke Neff, Jürgen Schlegel, and Matthias Riemenschneider. "P4-027: Altered gene expression in meningeal vessels of APP23 transgenic mice." Alzheimer's & Dementia 2 (July 2006): S521. http://dx.doi.org/10.1016/j.jalz.2006.05.1765.

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31

VLOEBERGHS, E., D. VANDAM, F. FRANCK, M. STAUFENBIEL, and P. DEDEYN. "Mood and male sexual behaviour in the APP23 model of Alzheimer's disease." Behavioural Brain Research 180, no. 2 (2007): 146–51. http://dx.doi.org/10.1016/j.bbr.2007.03.002.

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32

Van Acker, Zoë P., Evi Luyckx, Wendy Van Leuven, et al. "Impaired hypoxic tolerance in APP23 mice: a dysregulation of neuroprotective globin levels." FEBS Letters 591, no. 10 (2017): 1321–32. http://dx.doi.org/10.1002/1873-3468.12651.

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33

Polito, Letizia, Armando Chierchia, Marta Tunesi, et al. "Environmental Enrichment Lessens Cognitive Decline in APP23 Mice Without Affecting Brain Sirtuin Expression." Journal of Alzheimer's Disease 42, no. 3 (2014): 851–64. http://dx.doi.org/10.3233/jad-131430.

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34

Vloeberghs, E., D. Van Dam, S. Engelborghs, G. Nagels, M. Staufenbiel, and P. P. De Deyn. "P68 ALTERED CIRCADIAN LOCOMOTOR ACTIVITY IN APP23 MICE: A MODEL FOR BPSD DISTURBANCES." Behavioural Pharmacology 15, no. 5 (2004): A28. http://dx.doi.org/10.1097/00008877-200409000-00108.

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35

Van Ginneken, Chris, Karl-Herbert Schäfer, Debby Van Dam, Véronique Huygelen, and Peter P. De Deyn. "Morphological changes in the enteric nervous system of aging and APP23 transgenic mice." Brain Research 1378 (March 2011): 43–53. http://dx.doi.org/10.1016/j.brainres.2011.01.030.

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36

Frank, Stefanie, Guido J. Burbach, Michael Bonin, et al. "TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice." Glia 56, no. 13 (2008): 1438–47. http://dx.doi.org/10.1002/glia.20710.

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37

Hu, Xinran, Ryuta Morihara, Yusuke Fukui та ін. "Spearmint extract Neumentix downregulates amyloid-β accumulation by promoting phagocytosis in APP23 mice". Brain Research 1863 (вересень 2025): 149752. https://doi.org/10.1016/j.brainres.2025.149752.

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38

Mahler, Jasmin, Jose Morales-Corraliza, Julia Stolz та ін. "Endogenous murine Aβ increases amyloid deposition in APP23 but not in APPPS1 transgenic mice". Neurobiology of Aging 36, № 7 (2015): 2241–47. http://dx.doi.org/10.1016/j.neurobiolaging.2015.03.011.

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39

Büchner, M., R. Huber, C. Sturchler-Pierrat, M. Staufenbiel, and M. W. Riepe. "Impaired hypoxic tolerance and altered protein binding of NADH in presymptomatic APP23 transgenic mice." Neuroscience 114, no. 2 (2002): 285–89. http://dx.doi.org/10.1016/s0306-4522(02)00280-4.

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40

Boncristiano, Sonia, Michael E. Calhoun, Victor Howard, et al. "Neocortical synaptic bouton number is maintained despite robust amyloid deposition in APP23 transgenic mice." Neurobiology of Aging 26, no. 5 (2005): 607–13. http://dx.doi.org/10.1016/j.neurobiolaging.2004.06.010.

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41

Van Dam, Debby, and Peter Paul De Deyn. "Cognitive evaluation of disease-modifying efficacy of Galantamine and Memantine in the APP23 model." European Neuropsychopharmacology 16, no. 1 (2006): 59–69. http://dx.doi.org/10.1016/j.euroneuro.2005.06.005.

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42

Decourt, Boris, Aaron Walker, Mimi Macias, Amanda Gonzales, and Marwan Sabbagh. "P1-031: Lenalidomide as an antineuroinflammatory and BACE1 inhibitor: Pilot study on APP23 mice." Alzheimer's & Dementia 9 (July 2013): P163. http://dx.doi.org/10.1016/j.jalz.2013.05.251.

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43

Vlkolinsky, R., E. Titova, T. Krucker, et al. "Exposure to56Fe-Particle Radiation Accelerates Electrophysiological Alterations in the Hippocampus of APP23 Transgenic Mice." Radiation Research 173, no. 3 (2010): 342–52. http://dx.doi.org/10.1667/rr1825.1.

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44

Marutle, A., M. Ohmitsu, M. Nilbratt, N. H. Greig, A. Nordberg, and K. Sugaya. "Modulation of human neural stem cell differentiation in Alzheimer (APP23) transgenic mice by phenserine." Proceedings of the National Academy of Sciences 104, no. 30 (2007): 12506–11. http://dx.doi.org/10.1073/pnas.0705346104.

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45

Beckmann, Nicolau, Alexandra Schuler, Thomas Mueggler, et al. "Age-Dependent Cerebrovascular Abnormalities and Blood Flow Disturbances in APP23 Mice Modeling Alzheimer's Disease." Journal of Neuroscience 23, no. 24 (2003): 8453–59. http://dx.doi.org/10.1523/jneurosci.23-24-08453.2003.

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46

Van Erum, Jan, Debby Van Dam, Rishi Sheorajpanday, and Peter Paul De Deyn. "Sleep architecture changes in the APP23 mouse model manifest at onset of cognitive deficits." Behavioural Brain Research 373 (November 2019): 112089. http://dx.doi.org/10.1016/j.bbr.2019.112089.

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47

Senechal, Yann, Laetitia Prut, Peter H. Kelly, et al. "Increased exploratory activity of APP23 mice in a novel environment is reversed by siRNA." Brain Research 1243 (December 2008): 124–33. http://dx.doi.org/10.1016/j.brainres.2008.09.024.

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48

Koldamova, Radosveta, Matthias Staufenbiel, and Iliya Lefterov. "Lack of ABCA1 Considerably Decreases Brain ApoE Level and Increases Amyloid Deposition in APP23 Mice." Journal of Biological Chemistry 280, no. 52 (2005): 43224–35. http://dx.doi.org/10.1074/jbc.m504513200.

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49

Kawahara, Kohichi, Kentaro Nishi, Michita Suenobu та ін. "Oral Administration of Synthetic Retinoid Am80 (Tamibarotene) Decreases Brain β-Amyloid Peptides in APP23 Mice". Biological & Pharmaceutical Bulletin 32, № 7 (2009): 1307–9. http://dx.doi.org/10.1248/bpb.32.1307.

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Burbach, Guido J., Andreas Vlachos, Estifanos Ghebremedhin та ін. "Vessel ultrastructure in APP23 transgenic mice after passive anti-Aβ immunotherapy and subsequent intracerebral hemorrhage". Neurobiology of Aging 28, № 2 (2007): 202–12. http://dx.doi.org/10.1016/j.neurobiolaging.2005.12.003.

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