Relevant bibliographies by topics / APP23

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'APP23'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "APP23"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "APP23"

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Hartl, Daniela. "Proteomanalyse eines Mausmodells für die Alzheimer-Krankheit." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15892.

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Im Zentrum der vorliegenden Arbeit steht die Proteomanalyse des APP23-Mausmodells für die Alzheimer-Krankheit (AK). Es wurden die Gehirnregionen Hippocampus und Cortex der Altersstadien Embryonaltag 16 sowie 1, 2, 7 und 15 Monate untersucht und somit erstmals eine Art „Proteom-Lebensprofil“ eines Mausmodells erstellt. Bei dem Vergleich der APP23-Mäuse mit Wildtypmäusen konnte innnerhalb aller untersuchten Altersstadien und Gehirnregionen eine große Anzahl quantitativer Proteinexpressionsunterschiede festgestellt werden. Interessanterweise bestand jedoch im Hippocampus adoleszenter, zwei Monat
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Pahl, Julia Madeleine [Verfasser]. "Protective and curative effects of passive immunization against Amyloid-β protein in APP23 transgenic mice / Julia Madeleine Pahl". Ulm : Universität Ulm, 2017. http://d-nb.info/1133171435/34.

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Giunta, M. "RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/150259.

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Among pathologies of the old people, dementia represent one of the main sanitary problems. Approximately 70% of the dementia cases it is represented by the Alzheimer’s Disease, a neurodegenerative cerebral pathology, whose prevalence is supposed to be increased in the next years. One pathological hallmark is represented by amyloid-beta (Aβ) plaques, which represent the key element to oxidative and pro-inflammatory mechanisms by the activated microglia. The interaction, in fact, between activated microglia and plaques of Aβ induces the release of pro-inflammatory citokynes, like interleukin-6 (
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Frank, Stefanie [Verfasser]. "Charakterisierung der Amyloidplaque-assoziierten Entzündungsreaktion in APP23 transgenen Mäusen / von Stefanie Frank." 2009. http://d-nb.info/996684980/34.

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Books on the topic "APP23"

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Rules of Court App28 (Blue). Stationery Office Books, 1987.

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Book chapters on the topic "APP23"

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Van Dam, Debby, and Peter Paul De Deyn. "APP-Based Transgenic Models: The APP23 Model." In Neuromethods. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-898-0_20.

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"Appendix 11a: Calculus Example 1." In Clinical Psychometrics. John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118511800.app23.

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"Prophylaxis." In Oral Medicine and Medically Complex Patients. John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118783467.app23.

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"Preventive handling and restraint exercises." In Canine and Feline Behavior for Veterinary Technicians and Nurses. John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119421412.app23.

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"Appendix W: Inherited Eye Diseases in Food Animals." In Essentials of Veterinary Ophthalmology. John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118910337.app23.

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"Large Scale Medical Supply List." In Veterinary Forensics: Animal Cruelty Investigations. John Wiley & Sons, Inc.,, 2013. http://dx.doi.org/10.1002/9781118704738.app23.

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"Game Theory." In Warranty Fraud Management: Reducing Fraud and Other Excess Costs in Warranty and Service Operations. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781119277576.app03.

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"Satisfaction Survey for a Finance Team." In The Financial Controller and CFO's Toolkit. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781119291305.app03.

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"Charts and Volatility Studies." In Essential Option Strategies. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781119291558.app03.

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"C: Principal Central Screw Triple Combination." In Advanced Dynamics. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470950029.app03.

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Conference papers on the topic "APP23"

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Hugeng, Hugeng, A. M. Rivaldo, and H. S. Utama. "Building android application for smart agricultural system based on MIT inventor App2." In SIXTH INTERNATIONAL CONFERENCE OF MATHEMATICAL SCIENCES (ICMS 2022). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0126146.

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Shen, John Paul, Ana Bojorquez-Gomez, Justin Huang, et al. "Abstract AP23: A PLATINUM–RESISTANT SUBTYPE OF HIGH–GRADE SEROUS OVARIAN CANCER IDENTIFIED BY A NETWORK OF SOMATIC MUTATIONS." In Abstracts: 11th Biennial Ovarian Cancer Research Symposium; September 12-13, 2016; Seattle, WA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.ovcasymp16-ap23.

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Hooda, Jagmohan, Marián Novak, Matthew P. Salomon, et al. "Abstract AP23: EARLY LOSS OF MONOUBIQUITYLATION OF HISTONE H2B ALTERS KEY IMMUNE SIGNALING PATHWAYS PROMOTING THE PROGRESSION OF HIGH-GRADE SEROUS OVARIAN CANCER." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-ap23.

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Journal articles
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