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Journal articles on the topic 'APPswe mice'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Fu, Lu, Yao Sun, Yongqing Guo, et al. "Progressive Spatial Memory Impairment, Brain Amyloid Deposition and Changes in Serum Amyloid Levels as a Function of Age in APPswe/PS1dE9 Mice." Current Alzheimer Research 15, no. 11 (2018): 1053–61. http://dx.doi.org/10.2174/1567205015666180709112327.

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Background: Mice co-expressing human amyloid precursor protein with the Swedish mutation (APPswe) and exon-9-deleted presenilin (PS1dE9) has become one of the most widely used mouse models for studying Alzheimer’s disease (AD) pathogenesis and preclinical studies of AD therapeutic approaches. Objective: In this study, we systematically investigated cognitive decline, amyloid-β (Aβ) deposition and cerebral or Aβ serum levels as well as the relationships among these measures in APPswe/PS1dE9 transgenic mice. Method: APPswe/PS1dE9 mice were separated into four equal age cohorts (4, 6, 9, and 12 m

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2

Rodriguez-Vieitez, Elena, Ruiqing Ni, Balázs Gulyás, et al. "Astrocytosis precedes amyloid plaque deposition in Alzheimer APPswe transgenic mouse brain: a correlative positron emission tomography and in vitro imaging study." Eur J Nucl Med Mol Imaging. 42, no. 7 (2015): 1119–32. https://doi.org/10.1007/s00259-015-3047-0.

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PURPOSE: Pathological studies suggest that neuroinflammation is exacerbated by increased beta-amyloid (Aβ) levels in the brain early in Alzheimer's disease (AD). The time course and relationships between astrocytosis and Aβ deposition were examined using multitracer in vivo positron emission tomography (PET) imaging in an AD transgenic mouse model, followed by postmortem autoradiography and immunohistochemistry analysis. METHODS: PET imaging with the amyloid plaque tracer (11)C-AZD2184 and the astroglial tracer (11)C-deuterium-L-deprenyl ((11)C-DED) was carried out in APPswe mice

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Chen, Fang, Yingkun He, Pengwen Wang, et al. "Banxia Xiexin decoction ameliorated cognition via the regulation of insulin pathways and glucose transporters in the hippocampus of APPswe/PS1dE9 mice." International Journal of Immunopathology and Pharmacology 32 (January 1, 2018): 205873841878006. http://dx.doi.org/10.1177/2058738418780066.

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Reduced glucose utilization and deficient energy metabolism that occur in the early stages of Alzheimer’s disease correlate with impaired cognition, and this information is evidence that Alzheimer’s disease is a metabolic disease that is associated with brain insulin/insulin-like growth factor resistance. This research aimed to investigate the effects of Banxia Xiexin decoction (BXD) on cognitive deficits in APPswe/PS1dE9 double transgenic mice and verify the hypothesis that BXD treatment improves cognitive function via improving insulin signalling, glucose metabolism and synaptic plasticity i

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Lysikova, E. A., E. V. Kuzubova, A. I. Radchenko, et al. "APPswe/PS1dE9/Blg Transgenic Mouse Line for Modeling Cerebral Amyloid Angiopathy in Alzheimer’s Disease." Молекулярная биология 57, no. 1 (2023): 85–94. http://dx.doi.org/10.31857/s0026898423010081.

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Alzheimer’s disease (AD) is the most common proteinopathy, which is accompanied by a steady decrease in the patient’s cognitive functions with simultaneous accumulation of extracellular aggregates of amyloid β (Aβ) – amyloid plaques in the brain tissues and associated with neuroinflammation and neurodegeneration. Unlike humans and all other mammals, rats and mice have three amino acid substitutions in Aβ and do not reproduce the Alzheimer’s pathology. However, the appearance of amyloid plaques is observed in the brains of transgenic mice with the overexpression of human Aβ, which makes it poss

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Wang, Ruonan, Shijia Kang, Zirui Zhao, et al. "Chicoric Acid Ameliorated Beta-Amyloid Pathology and Enhanced Expression of Synaptic-Function-Related Markers via L1CAM in Alzheimer’s Disease Models." International Journal of Molecular Sciences 25, no. 6 (2024): 3408. http://dx.doi.org/10.3390/ijms25063408.

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Alzheimer’s disease (AD) is the most common progressive neurodegenerative disease. The accumulation of amyloid-beta (Aβ) plaques is a distinctive pathological feature of AD patients. The aims of this study were to evaluate the therapeutic effect of chicoric acid (CA) on AD models and to explore its underlying mechanisms. APPswe/Ind SH-SY5Y cells and 5xFAD mice were treated with CA. Soluble Aβ1–42 and Aβ plaque levels were analyzed by ELISA and immunohistochemistry, respectively. Transcriptome sequencing was used to compare the changes in hippocampal gene expression profiles among the 5xFAD mou

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Stenzel, J., C. Rühlmann, T. Lindner, et al. "[18F]-florbetaben PET/CT Imaging in the Alzheimer’s Disease Mouse Model APPswe/PS1dE9." Current Alzheimer Research 16, no. 1 (2018): 49–55. http://dx.doi.org/10.2174/1567205015666181022095904.

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Background: Positron-emission-tomography (PET) using 18F labeled florbetaben allows noninvasive in vivo-assessment of amyloid-beta (Aβ), a pathological hallmark of Alzheimer’s disease (AD). In preclinical research, [<sup>18</sup>F]-florbetaben-PET has already been used to test the amyloid-lowering potential of new drugs, both in humans and in transgenic models of cerebral amyloidosis. The aim of this study was to characterize the spatial pattern of cerebral uptake of [<sup>18</sup>F]-florbetaben in the APPswe/ PS1dE9 mouse model of AD in comparison to histologically det

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7

Doméné, Aurélie, Chelsea Cavanagh, Guylène Page, et al. "Expression of Phenotypic Astrocyte Marker Is Increased in a Transgenic Mouse Model of Alzheimer’s Disease versus Age-Matched Controls: A Presymptomatic Stage Study." International Journal of Alzheimer's Disease 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/5696241.

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Recent mouse studies of the presymptomatic stage of Alzheimer’s disease (AD) have suggested that proinflammatory changes, such as glial activation and cytokine induction, may occur already at this early stage through unknown mechanisms. Because TNFαcontributes to increased Aβproduction from the Aβprecursor protein (APP), we assessed a putative correlation between APP/Aβand TNFαduring the presymptomatic stage as well as early astrocyte activation in the hippocampus of 3-month-old APPswe/PS1dE9 mice. While Western blots revealed significant APP expression, Aβwas not detectable by Western blot or

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8

Tsay, Huey-Jen, Hui-Kang Liu, Yueh-Hsiung Kuo, et al. "EK100 and Antrodin C Improve Brain Amyloid Pathology in APP/PS1 Transgenic Mice by Promoting Microglial and Perivascular Clearance Pathways." International Journal of Molecular Sciences 22, no. 19 (2021): 10413. http://dx.doi.org/10.3390/ijms221910413.

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Alzheimer’s disease (AD) is characterized by the deposition of β-amyloid peptide (Aβ). There are currently no drugs that can successfully treat this disease. This study first explored the anti-inflammatory activity of seven components isolated from Antrodia cinnamonmea in BV2 cells and selected EK100 and antrodin C for in vivo research. APPswe/PS1dE9 mice were treated with EK100 and antrodin C for one month to evaluate the effect of these reagents on AD-like pathology by nesting behavior, immunohistochemistry, and immunoblotting. Ergosterol and ibuprofen were used as control. EK100 and antrodi

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9

Metaxas, Athanasios, Ramanan Vaitheeswaran, Katrine T. Jensen, et al. "Reduced Serotonin Transporter Levels and Inflammation in the Midbrain Raphe of 12 Month Old APPswe/PSEN1dE9 Mice." Current Alzheimer Research 15, no. 5 (2018): 420–28. http://dx.doi.org/10.2174/1567205014666171004113537.

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Background: Although mood and sleep disturbances are nearly universal among patients with Alzheimer's disease (AD), brain structures involved in non-cognitive processing remain under characterized in terms of AD pathology. Objectives: This study was designed to evaluate hallmarks of AD pathology in the brainstem of the APPswe/PS1dE9 mouse model of familial AD. Methods: Fresh-frozen sections from female, 12 month old, transgenic and control B6C3 mice (n=6/genotype) were examined for amyloid burden and neurofibrillary alterations, by using 6E10 immunohistochemistry and the Gallyas silver stain,

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Zamarbide, Marta, Eva Martinez-Pinilla, Francisco Gil-Bea, Masashi Yanagisawa, Rafael Franco, and Alberto Perez-Mediavilla. "Genetic Inactivation of Free Fatty Acid Receptor 3 Impedes Behavioral Deficits and Pathological Hallmarks in the APPswe Alzheimer’s Disease Mouse Model." International Journal of Molecular Sciences 23, no. 7 (2022): 3533. http://dx.doi.org/10.3390/ijms23073533.

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The free fatty acid FFA3 receptor (FFA3R) belongs to the superfamily of G-protein-coupled receptors (GPCRs). In the intestine and adipose tissue, it is involved in the regulation of energy metabolism, but its function in the brain is unknown. We aimed, first, to investigate the expression of the receptor in the hippocampus of Alzheimer disease (AD) patients at different stages of the disease and, second, to assess whether genetic inactivation of the Ffar3 gene could affect the phenotypic features of the APPswe mouse model. The expression of transcripts for FFA receptors in postmortem human hip

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11

Bednar, Ivan, David Paterson, Amelia Marutle, et al. "Selective Nicotinic Receptor Consequences in APPSWE Transgenic Mice." Molecular and Cellular Neuroscience 20, no. 2 (2002): 354–65. http://dx.doi.org/10.1006/mcne.2002.1112.

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12

Lin, Xiao, and Li Yu. "Effect of Plant Compound Curcumin on the Expression of a-Synuclein in Hippocampal Neurons of APPswe/PS1dE9 Double Transgenic Mice." Advanced Materials Research 781-784 (September 2013): 643–46. http://dx.doi.org/10.4028/www.scientific.net/amr.781-784.643.

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In this study, we aim to investigate the effect of curcumin on the expression of a-synuclein in the APPswe/PS1dE9 double transgenic mice. APPswe/PS1dE9 double transgenic mice were used as AD (Alzheimer's disease) model and fed with different concentrations of curcumin every day for 6 months, then immunohistochemistry method were used to detect the expression of a-synuclein in hippocampus of mice. The expression of a-syn in hippocampal neuron was decreased significantly after treated with 0.16g/kg to 1.0g/kg curcumin, the change was apparent in dose-dependent manner (P<0.05). a-synuclein pay

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13

Chouliaras, Leonidas, Roy Lardenoije, Gunter Kenis, et al. "Age-related disturbances in DNA (hydroxy)methylation in APP/PS1 mice." Translational Neuroscience 9, no. 1 (2018): 190–202. http://dx.doi.org/10.1515/tnsci-2018-0028.

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Abstract Brain aging has been associated with aberrant DNA methylation patterns, and changes in the levels of DNA methylation and associated markers have been observed in the brains of Alzheimer’s disease (AD) patients. DNA hydroxymethylation, however, has been sparsely investigated in aging and AD. We have previously reported robust decreases in 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) in the hippocampus of AD patients compared to non-demented controls. In the present study, we investigated 3- and 9-month-old APPswe/PS1ΔE9 transgenic and wild-type mice for possible age-rela

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14

Broberg, Dana N., Dickson Wong, Miranda Bellyou, et al. "Effects of Memantine and High Dose Vitamin D on Gait in Male APP/PS1 Alzheimer’s Disease Mice Following Vitamin D Deprivation." Journal of Alzheimer's Disease 85, no. 4 (2022): 1755–66. http://dx.doi.org/10.3233/jad-215188.

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Background: Altered gait is a frequent feature of Alzheimer’s disease (AD), as is vitamin D deficiency. Treatment with memantine and vitamin D can protect cortical axons from exposure to amyloid-β and glutamate toxicity, suggesting this combination may mitigate altered gait in AD. Objective: Investigate the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on gait performance in APPswe/PS1dE9 mice. Methods: Male APPswe/PS1dE9 mice were split into four groups (n = 14 each) at 2.5 months of age. A control group was fed a standard diet throughout wh

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15

He, Yingkun, Pengwen Wang, Peng Wei, et al. "Effects of curcumin on synapses in APPswe/PS1dE9 mice." International Journal of Immunopathology and Pharmacology 29, no. 2 (2016): 217–25. http://dx.doi.org/10.1177/0394632016638099.

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16

Chen, Fang, Yingkun He, Pengwen Wang, et al. "Curcumin can influence synaptic dysfunction in APPswe/PS1dE9 mice." Journal of Traditional Chinese Medical Sciences 5, no. 2 (2018): 168–76. http://dx.doi.org/10.1016/j.jtcms.2018.03.005.

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17

Machová, E., J. Jakubík, P. Michal, et al. "Impairment of muscarinic transmission in transgenic APPswe/PS1dE9 mice." Neurobiology of Aging 29, no. 3 (2008): 368–78. http://dx.doi.org/10.1016/j.neurobiolaging.2006.10.029.

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18

Witucki, Łukasz, and Hieronim Jakubowski. "Depletion of Paraoxonase 1 (Pon1) Dysregulates mTOR, Autophagy, and Accelerates Amyloid Beta Accumulation in Mice." Cells 12, no. 5 (2023): 746. http://dx.doi.org/10.3390/cells12050746.

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Paraoxonase 1 (PON1), a homocysteine (Hcy)-thiolactone detoxifying enzyme, has been associated with Alzheimer’s disease (AD), suggesting that PON1 plays an important protective role in the brain. To study the involvement of PON1 in the development of AD and to elucidate the mechanism involved, we generated a new mouse model of AD, the Pon1−/−xFAD mouse, and examined how Pon1 depletion affects mTOR signaling, autophagy, and amyloid beta (Aβ) accumulation. To elucidate the mechanism involved, we examined these processes in N2a-APPswe cells. We found that Pon1 depletion significantly downregulate

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19

Müller, Luisa, Timo Kirschstein, Rüdiger Köhling, Angela Kuhla, and Stefan Teipel. "Neuronal Hyperexcitability in APPSWE/PS1dE9 Mouse Models of Alzheimer’s Disease." Journal of Alzheimer's Disease 81, no. 3 (2021): 855–69. http://dx.doi.org/10.3233/jad-201540.

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Transgenic mouse models serve a better understanding of Alzheimer’s disease (AD) pathogenesis and its consequences on neuronal function. Well-known and broadly used AD models are APPswe/PS1dE9 mice, which are able to reproduce features of amyloid-β (Aβ) plaque formations as well as neuronal dysfunction as reflected in electrophysiological recordings of neuronal hyperexcitability. The most prominent findings include abnormal synaptic function and synaptic reorganization as well as changes in membrane threshold and spontaneous neuronal firing activities leading to generalized excitation-inhibiti

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20

Varela-Nallar, Lorena, Sebastian B. Arredondo, Cheril Tapia-Rojas, Juan Hancke, and Nibaldo C. Inestrosa. "Andrographolide Stimulates Neurogenesis in the Adult Hippocampus." Neural Plasticity 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/935403.

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Andrographolide (ANDRO) is a labdane diterpenoid component ofAndrographis paniculatawidely used for its anti-inflammatory properties. We have recently determined that ANDRO is a competitive inhibitor of glycogen synthase kinase-3β(GSK-3β), a key enzyme of the Wnt/β-catenin signaling cascade. Since this signaling pathway regulates neurogenesis in the adult hippocampus, we evaluated whether ANDRO stimulates this process. Treatment with ANDRO increased neural progenitor cell proliferation and the number of immature neurons in the hippocampus of 2- and 10-month-old mice compared to age-matched con

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Gonzalo-Gobernado, Rafael, Juan Perucho, Manuela Vallejo-Muñoz, et al. "Liver Growth Factor “LGF” as a Therapeutic Agent for Alzheimer’s Disease." International Journal of Molecular Sciences 21, no. 23 (2020): 9201. http://dx.doi.org/10.3390/ijms21239201.

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Alzheimer’s disease (AD) is a progressive degenerative disorder and the most common cause of dementia in aging populations. Although the pathological hallmarks of AD are well defined, currently no effective therapy exists. Liver growth factor (LGF) is a hepatic albumin–bilirubin complex with activity as a tissue regenerating factor in several neurodegenerative disorders such as Parkinson’s disease and Friedreich’s ataxia. Our aim here was to analyze the potential therapeutic effect of LGF on the APPswe mouse model of AD. Twenty-month-old mice received intraperitoneal (i.p.) injections of 1.6 µ

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22

Malm, Tarja, Jari Koistinaho, and Katja Kanninen. "Utilization of APPswe/PS1dE9 Transgenic Mice in Research of Alzheimer's Disease: Focus on Gene Therapy and Cell-Based Therapy Applications." International Journal of Alzheimer's Disease 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/517160.

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One of the most extensively used transgenic mouse model of Alzheimer’s disease (AD) is APPswe/PS1dE9 mice, which over express the Swedish mutation of APP together with PS1 deleted in exon 9. These mice show increase in parenchymal Aβload with Aβplaques starting from the age of four months, glial activation, and deficits in cognitive functions at the age of 6 months demonstrated by radial arm water maze and 12-13 months seen with Morris Water Maze test. As gene transfer technology allows the delivery of DNA into target cells to achieve the expression of a protective or therapeutic protein, and

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Cheng, David, Jac Kee Low, Warren Logge, Brett Garner та Tim Karl. "Novel behavioural characteristics of female APPSwe/PS1ΔE9 double transgenic mice". Behavioural Brain Research 260 (березень 2014): 111–18. http://dx.doi.org/10.1016/j.bbr.2013.11.046.

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Good, Mark A., Gemma Hale, and Victoria Staal. "Impaired "episodic-like" object memory in adult APPswe transgenic mice." Behavioral Neuroscience 121, no. 2 (2007): 443–48. http://dx.doi.org/10.1037/0735-7044.121.2.443.

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Huang, Huang, Sipei Nie, Min Cao, et al. "Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice." AGE 38, no. 4 (2016): 303–22. http://dx.doi.org/10.1007/s11357-016-9929-7.

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26

Wang, Fei, Xueyan Shen, Shuping Li, et al. "Splenocytes derived from young WT mice prevent AD progression in APPswe/PSENldE9 transgenic mice." Oncotarget 6, no. 25 (2015): 20851–62. http://dx.doi.org/10.18632/oncotarget.4930.

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27

Joly, Sandrine, Léa Rodriguez та Vincent Pernet. "The Lack of Amyloidogenic Activity Is Persistent in Old WT and APPswe/PS1ΔE9 Mouse Retinae". International Journal of Molecular Sciences 22, № 21 (2021): 11344. http://dx.doi.org/10.3390/ijms222111344.

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We have previously reported that vision decline was not associated with amyloidogenesis processing in aging C57BL/6J wild-type (WT) mice and in a mouse model of Alzheimer’s disease, the APPswe/PS1ΔE9 transgenic mouse model (APP/PS1). This conclusion was drawn using middle-aged (10–13 months old) mice. Here, we hypothesized that compared with hippocampal and cortical neurons, the weak amyloidogenic activity of retinal neurons may result in a detectable release of amyloid β (Aβ) only in aged mice, i.e., between 14 and 24 months of age. The aim of the present study was thus to follow potential ac

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Yu, Linjie, Yi Liu, Yuexinzi Jin, et al. "Lentivirus-Mediated HDAC3 Inhibition Attenuates Oxidative Stress in APPswe/PS1dE9 Mice." Journal of Alzheimer's Disease 61, no. 4 (2018): 1411–24. http://dx.doi.org/10.3233/jad-170844.

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Taniuchi, Nobuhiko, Tetsuhiro Niidome, Yasuaki Goto, Akinori Akaike, Takeshi Kihara, and Hachiro Sugimoto. "Decreased proliferation of hippocampal progenitor cells in APPswe/PS1dE9 transgenic mice." NeuroReport 18, no. 17 (2007): 1801–5. http://dx.doi.org/10.1097/wnr.0b013e3282f1c9e9.

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Papadopoulos, Panayiota, Xin-Kang Tong та Edith Hamel. "Selective benefits of simvastatin in bitransgenic APPSwe,Ind/TGF-β1 mice". Neurobiology of Aging 35, № 1 (2014): 203–12. http://dx.doi.org/10.1016/j.neurobiolaging.2013.07.010.

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Ramos-Rodriguez, Juan Jose, Oscar Ortiz-Barajas, Carlos Gamero-Carrasco, et al. "Prediabetes-induced vascular alterations exacerbate central pathology in APPswe/PS1dE9 mice." Psychoneuroendocrinology 48 (October 2014): 123–35. http://dx.doi.org/10.1016/j.psyneuen.2014.06.005.

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Barnes, Philip, Gemma Hale, and Mark Good. "Intramaze and Extramaze Cue Processing in Adult APPSWE Tg2576 Transgenic Mice." Behavioral Neuroscience 118, no. 6 (2004): 1184–95. http://dx.doi.org/10.1037/0735-7044.118.6.1184.

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Krivinko, Josh, Susan Erickson, Matthew MacDonald, Megan Garver, and Robert A. Sweet. "Fingolimod Treatment Rescues Psychosis-Associated Behavioral Aberrations in Appswe/Psen1de9 Mice." American Journal of Geriatric Psychiatry 26, no. 3 (2018): S144—S145. http://dx.doi.org/10.1016/j.jagp.2018.01.175.

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Rombaut, Ben, Melissa Schepers, Assia Tiane, et al. "Early Inhibition of Phosphodiesterase 4B (PDE4B) Instills Cognitive Resilience in APPswe/PS1dE9 Mice." Cells 13, no. 12 (2024): 1000. http://dx.doi.org/10.3390/cells13121000.

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Microglia activity can drive excessive synaptic loss during the prodromal phase of Alzheimer’s disease (AD) and is associated with lowered cyclic adenosine monophosphate (cAMP) due to cAMP phosphodiesterase 4B (PDE4B). This study aimed to investigate whether long-term inhibition of PDE4B by A33 (3 mg/kg/day) can prevent synapse loss and its associated cognitive decline in APPswe/PS1dE9 mice. This model is characterized by a chimeric mouse/human APP with the Swedish mutation and human PSEN1 lacking exon 9 (dE9), both under the control of the mouse prion protein promoter. The effects on cognitiv

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Utyro, Olga, Olga Włoczkowska-Łapińska, and Hieronim Jakubowski. "Association of GLOD4 with Alzheimer’s Disease in Humans and Mice." Journal of Alzheimer's Disease 101, no. 3 (2024): 823–34. http://dx.doi.org/10.3233/jad-240512.

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Background: Glyoxalase domain containing protein 4 (GLOD4), a protein of an unknown function, is associated with Alzheimer’s disease (AD). Three GLOD4 isoforms are known. The mechanism underlying GLOD4’s association with AD was unknown. Objective: To assess GLOD4’s role in the central nervous system by studying GLOD4 isoforms expression in human frontal cerebral cortical tissues from AD patients and in brains of Blmh–/–5xFAD mouse AD model of AD. Methods: GLOD4 protein and mRNA were quantified in human and mouse brains by western blotting and RT-qPCR, respectively. Mouse brain amyloid-β (Aβ) w

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Feng, Hui-li, Hui-zi Dang, Hui Fan, et al. "Curcumin ameliorates insulin signalling pathway in brain of Alzheimer’s disease transgenic mice." International Journal of Immunopathology and Pharmacology 29, no. 4 (2016): 734–41. http://dx.doi.org/10.1177/0394632016659494.

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Deficits in glucose, impaired insulin signalling and brain insulin resistance are common in the pathogenesis of Alzheimer’s disease (AD); therefore, some scholars even called AD type 3 diabetes mellitus. Curcumin can reduce the amyloid pathology in AD. Moreover, it is a well-known fact that curcumin has anti-oxidant and anti-inflammatory properties. However, whether or not curcumin could regulate the insulin signal transduction pathway in AD remains unclear. In this study, we used APPswe/PS1dE9 double transgenic mice as the AD model to investigate the mechanisms and the effects of curcumin on

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Wang, Hao, Fang-fang Zhang, Yong Xu, et al. "The Phosphodiesterase-4 Inhibitor Roflumilast, a Potential Treatment for the Comorbidity of Memory Loss and Depression in Alzheimer’s Disease: A Preclinical Study in APP/PS1 Transgenic Mice." International Journal of Neuropsychopharmacology 23, no. 10 (2020): 700–711. http://dx.doi.org/10.1093/ijnp/pyaa048.

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Abstract Background Depression is highly related to Alzheimer’s disease (AD), yet no effective treatment is available. Phosphodiesterase-4 (PDE4) has been considered a promising target for treatment of AD and depression. Roflumilast, the first PDE4 inhibitor approved for clinical use, improves cognition at doses that do not cause side effects such as emesis. Methods Here we examined the effects of roflumilast on behavioral dysfunction and the related mechanisms in APPswe/PS1dE9 transgenic mice, a widely used model of AD. Mice at 10 months of age were examined for memory in the novel object rec

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Tzeng, Te-Chen, Yuto Hasegawa, Risa Iguchi, et al. "Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice." Proceedings of the National Academy of Sciences 115, no. 36 (2018): 9002–7. http://dx.doi.org/10.1073/pnas.1801802115.

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Alzheimer’s disease (AD) is characterized by the progressive destruction and dysfunction of central neurons. AD patients commonly have unprovoked seizures compared with age-matched controls. Amyloid peptide-related inflammation is thought to be an important aspect of AD pathogenesis. We previously reported that NLRP3 inflammasome KO mice, when bred into APPswe/PS1ΔE9 (APP/PS1) mice, are completely protected from amyloid-induced AD-like disease, presumably because they cannot produce mature IL1β or IL18. To test the role of IL18, we bred IL18KO mice with APP/PS1 mice. Surprisingly, IL18KO/APP/P

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Jiang, Yanhua, Zhe Li, Hong Ma, et al. "Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice." Cellular Physiology and Biochemistry 46, no. 4 (2018): 1398–411. http://dx.doi.org/10.1159/000489155.

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Background/Aims: TREM2 plays a crucial role in modulating microglial function through interaction with DAP12, the adapter for TREM2. Emerging evidence has demonstrated that TREM2 could suppress neuroinflammatory responses by repression of microglia-mediated cytokine production. This study investigated the potential role of TREM2 in surgery-induced cognitive deficits and neuroinflammatory responses in wild-type (WT) and APPswe/PS1dE9 mice. Methods: Adult APPswe/PS1dE9 transgenic male mice (a classic transgenic model of Alzheimer’s disease, 3 months old) and their age-matched WT mice received in

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Omar, Syed, Christopher Scott, Adam Hamlin, and Hassan Obied. "Olive Biophenols Reduces Alzheimer’s Pathology in SH-SY5Y Cells and APPswe Mice." International Journal of Molecular Sciences 20, no. 1 (2018): 125. http://dx.doi.org/10.3390/ijms20010125.

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Alzheimer’s disease (AD) is a major neurodegenerative disease, associated with the hallmark proteinacious constituent called amyloid beta (Aβ) of senile plaques. Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. In order to reduce the Aβ plaque burden and overcome the side effects from the synthetic inhibitors, the current study was designed to focus on direct inhibition of with or without metal-induced Aβ fibril formation and aggregation by using olive biophenols. Exposure of neuroblastoma (SH-SY5Y) cells with Aβ42

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Liu, Quan Feng, Suganya Kanmani, Jinhyuk Lee, Geun-Woo Kim, Songhee Jeon та Byung-Soo Koo. "Neoline Improves Memory Impairment and Reduces Amyloid-β Level and Tau Phosphorylation Through AMPK Activation in the Mouse Alzheimer’s Disease Model". Journal of Alzheimer's Disease 81, № 2 (2021): 507–16. http://dx.doi.org/10.3233/jad-201614.

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Background: Alzheimer’s disease (AD) is the most general, chronic, and progressive neurodegenerative senile disorder characterized clinically by progressive cognitive deterioration and memory impairment. Neoline is effective against neuropathic pain models, but the effects of neoline against AD-like phenotypes have not been investigated. Objective: We offer the investigation of the effects of neoline in AD. Methods: In this study, a Tg-APPswe/PS1dE9 AD mouse model was treated orally with neoline at a concentration of 0.5 mg/kg or 0.1 mg/kg starting at 7.5 months and administered for three mont

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Sierksma, Annerieke S. R., Laurence de Nijs, Govert Hoogland, et al. "Fluoxetine Treatment Induces Seizure Behavior and Premature Death in APPswe/PS1dE9 Mice." Journal of Alzheimer's Disease 51, no. 3 (2016): 677–82. http://dx.doi.org/10.3233/jad-151066.

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Abbott, Ana C., Carla Calderon Toledo, Florencia C. Aranguiz, Nibaldo C. Inestrosa та Lorena Varela-Nallar. "Tetrahydrohyperforin Increases Adult Hippocampal Neurogenesis in Wild-Type and APPswe/PS1ΔE9 Mice". Journal of Alzheimer's Disease 34, № 4 (2013): 873–85. http://dx.doi.org/10.3233/jad-121714.

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Thériault, Peter, Ayman ElAli, and Serge Rivest. "High fat diet exacerbates Alzheimer's disease-related pathology in APPswe/PS1 mice." Oncotarget 7, no. 42 (2016): 67808–27. http://dx.doi.org/10.18632/oncotarget.12179.

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Perez, S. E. "Nigrostriatal Dysfunction in Familial Alzheimer's Disease-Linked APPswe/PS1 E9 Transgenic Mice." Journal of Neuroscience 25, no. 44 (2005): 10220–29. http://dx.doi.org/10.1523/jneurosci.2773-05.2005.

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Lalonde, R., H. D. Kim та K. Fukuchi. "Exploratory activity, anxiety, and motor coordination in bigenic APPswe + PS1/ΔE9 mice". Neuroscience Letters 369, № 2 (2004): 156–61. http://dx.doi.org/10.1016/j.neulet.2004.07.069.

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Nikolajsen, Gitte Nykjær, Kamila Anna Kotynski, Morten Skovgaard Jensen, and Mark J. West. "Quantitative analysis of the capillary network of aged APPswe/PS1dE9 transgenic mice." Neurobiology of Aging 36, no. 11 (2015): 2954–62. http://dx.doi.org/10.1016/j.neurobiolaging.2015.08.004.

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Krivinko, Josh M., Susan L. Erickson, Eric E. Abrahamson, et al. "Kalirin reduction rescues psychosis-associated behavioral deficits in APPswe/PSEN1dE9 transgenic mice." Neurobiology of Aging 54 (June 2017): 59–70. http://dx.doi.org/10.1016/j.neurobiolaging.2017.02.006.

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Morgan, Todd E., Nilay V. Patel, Neel Vora, Siroun Tahtakran, M. Paul Murphy та Caleb E. Finch. "P2-081 Caloric restriction slows Aβ-plaque deposition in APPSWE/IND mice". Neurobiology of Aging 25 (липень 2004): S247. http://dx.doi.org/10.1016/s0197-4580(04)80828-5.

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Zhang, P., M. Q. Xie, Y.-Q. Ding, et al. "Allopregnanolone enhances the neurogenesis of midbrain dopaminergic neurons in APPswe/PSEN1 mice." Neuroscience 290 (April 2015): 214–26. http://dx.doi.org/10.1016/j.neuroscience.2015.01.019.

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