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Journal articles on the topic 'PS1 mice'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Chen, Min, Jiashuo Zheng, Guohao Liu та ін. "High Dietary Iron Disrupts Iron Homeostasis and Induces Amyloid-β and Phospho-τ Expression in the Hippocampus of Adult Wild-Type and APP/PS1 Transgenic Mice". Journal of Nutrition 149, № 12 (2019): 2247–54. http://dx.doi.org/10.1093/jn/nxz168.

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ABSTRACT Background Brain iron deposition is a feature of Alzheimer disease and may contribute to its development. However, the relative contribution of dietary iron remains unclear. Objectives We investigated the impact of high dietary iron on brain pathological changes and cognitive function in adult wild-type (WT) mice and amyloid precursor protein/presenilin 1 (APP/PS1) double transgenic mice. Methods Male WT mice and APP/PS1 mice aged 10 wk were fed either a control diet (66 mg Fe/kg) (WT-Ctrl and APP/PS1-Ctrl) or a high iron diet (14 g Fe/kg) (WT-High Fe and APP/PS1-High Fe) for 20 wk. I

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Han, Bing, Jin-Hua Wang, Yuan Geng, et al. "Chronic Stress Contributes to Cognitive Dysfunction and Hippocampal Metabolic Abnormalities in APP/PS1 Mice." Cellular Physiology and Biochemistry 41, no. 5 (2017): 1766–76. http://dx.doi.org/10.1159/000471869.

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Background/Aims: Stress response is determined by the brain, and the brain is a sensitive target for stress. Our previous experiments have confirmed that once the stress response is beyond the tolerable limit of the brain, particularly that of the hippocampus, it will have deleterious effects on hippocampal structure and function; however, the metabolic mechanisms for this are not well understood. Methods: Here, we used morris water maze, elisa and gas chromatography-time of flight/mass spectrometry to observe the changes in cognition, neuropathology and metabolomics in the hippocampus of APP/

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Zha, Lihuang, Zaixin Yu, Jian Fang, Li Zhou, Wen Guo, and Jun Zhou. "NLRC3 Delays the Progression of AD in APP/PS1 Mice via Inhibiting PI3K Activation." Oxidative Medicine and Cellular Longevity 2020 (December 24, 2020): 1–14. http://dx.doi.org/10.1155/2020/5328031.

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NLRC3 inhibits inflammatory responses. Neuroinflammation induces and accelerates the onset of Alzheimer’s disease (AD). This study is aimed at investigating whether NLRC3 plays a role in neuroinflammation, Aβ accumulation, and neuroprotection in AD mice. 12-month-old APP/PS1 transgenic and C57 mice were used for studies in vivo. In vitro, organotypic hippocampal slices were cultured. We found that the expression of NLRC3 was downregulated in the brain tissues of APP/PS1 mice. Mice in the APP/PS1 group had a significant attenuation of learning and memory ability compared to the control group, a

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Zhang, Q. L., L. Jia, X. Jiao, et al. "APP/PS1 Transgenic Mice Treated with Aluminum: An Update of Alzheimer's Disease Model." International Journal of Immunopathology and Pharmacology 25, no. 1 (2012): 49–58. http://dx.doi.org/10.1177/039463201202500107.

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There is still no animal model available that can mimic all the cognitive, behavioral, biochemical, and histopathological abnormalities observed in patients with Alzheimer's disease (AD). We undertook to consider the interaction between genetic factors, including amyloid precursor protein (APP) and presenilin-1 (PS1), and environmental factors, such as Aluminum (Al) in determining susceptibility outcomes when studying the pathogenesis of AD. In this article, we provide an AD model in APP/PS1 transgenic mice triggered by Al. The animal model was established via intracerebral ventricular microin

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Kim, Jin Woo, Tong-Shin Chang, Ji Eun Lee, et al. "Negative Regulation of the Sapk/Jnk Signaling Pathway by Presenilin 1." Journal of Cell Biology 153, no. 3 (2001): 457–64. http://dx.doi.org/10.1083/jcb.153.3.457.

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Presenilin 1 (PS1) plays a pivotal role in Notch signaling and the intracellular metabolism of the amyloid β-protein. To understand intracellular signaling events downstream of PS1, we investigated in this study the action of PS1 on mitogen-activated protein kinase pathways. Overexpressed PS1 suppressed the stress-induced stimulation of stress-activated protein kinase (SAPK)/c-Jun NH2-terminal kinase (JNK) in human embryonic kidney 293 cells. Interestingly, two functionally inactive PS1 mutants, PS1(D257A) and PS1(D385A), failed to inhibit UV-stimulated SAPK/JNK. Furthermore, H2O2- or UV-stimu

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Li, Dan, Chen Wang, Song Tan, and Yu Li. "Plant Compound Curcumin Increased the Expression of MAP2 in Hippocampal Neurons of APPswe/PS1dE9 Double Transgenic Mice." Advanced Materials Research 781-784 (September 2013): 717–20. http://dx.doi.org/10.4028/www.scientific.net/amr.781-784.717.

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In this study, we aim to investigate the effect of curcumin on the expression of MAP2 in hippocampus in APP/PS1 double transgenic mice. AD model was established with APP/PS1 double transgenic mice, which were fed for 6 months with different concentration of curcumin diet. Immunohistochemistry were applied to evaluate the expressive of MAP2 in hippocampus of transgenic mice. The expression of MAP2 in hippocampus were decreased in APP/PS1 double transgenic mice, but increased in concentration-dependent manner in curcumin treatment group,especially in CA1 and CA3 region. MAP2 may play an importan

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Brown, Desmond, Gobinda Sarkar, Teresa Decklever та ін. "SCIDOT-39. K16ApoE ENHANCES Aβ-ASSOCIATED 11C-PiB DEPOSITION AND PET SIGNAL IN APP/PS1 TRANSGENIC MICE". Neuro-Oncology 21, Supplement_6 (2019): vi279—vi280. http://dx.doi.org/10.1093/neuonc/noz175.1175.

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Abstract OBJECTIVE The K16ApoE peptide enhances delivery of multiple agents across the blood-brain barrier (BBB). Transgenic mouse models are central to elucidating the underlying pathophysiology of Alzheimer’s Disease (AD) and provide a system for evaluating novel therapeutic strategies. PET imaging plays a central clinical role in diagnosing human cases of AD but has had variable performance in mouse models. We investigated the role of K16ApoE to enhance delivery of a radiolabeled PET imaging tracer, 11C-PiB and assess whether this corresponds to improved PET sensitivity in APP/PS1 transgeni

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Leitner, Nicole R., Thomas Kolbe, Caroline Lassnig, Konrad Hochedlinger, Thomas Rülicke, and Mathias Müller. "PS1-69 Inducible STAT1 protein in mice." Cytokine 52, no. 1-2 (2010): 31–32. http://dx.doi.org/10.1016/j.cyto.2010.07.141.

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Lee, Yi-Heng, Hao-Chieh Hsu, Pei-Chen Kao, et al. "Augmented Insulin and Leptin Resistance of High Fat Diet-Fed APPswe/PS1dE9 Transgenic Mice Exacerbate Obesity and Glycemic Dysregulation." International Journal of Molecular Sciences 19, no. 8 (2018): 2333. http://dx.doi.org/10.3390/ijms19082333.

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Alzheimer’s disease (AD), a progressive neurodegenerative disease is highly associated with metabolic syndromes. We previously demonstrated that glycemic dysregulation and obesity are augmented in high fat diet (HFD)-treated APPswe/PS1dE9 (APP/PS1) transgenic mice. In the current study, the underlying mechanism mediating exacerbated metabolic stresses in HFD APP/PS1 transgenic mice was further examined. APP/PS1 mice developed insulin resistance and, consequently, impaired glucose homeostasis after 10 weeks on HFD. [18F]-2-fluoro-2-deoxy-d-glucose ([18F]-FDG) positron emission tomography showed

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Yuan, Li, Jun Zhang, Jun-Hong Guo, et al. "DAla2-GIP-GLU-PAL Protects Against Cognitive Deficits and Pathology in APP/PS1 Mice by Inhibiting Neuroinflammation and Upregulating cAMP/PKA/CREB Signaling Pathways." Journal of Alzheimer's Disease 80, no. 2 (2021): 695–713. http://dx.doi.org/10.3233/jad-201262.

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Background: Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive decline in cognitive function. Type 2 diabetes mellitus (T2DM) is an important risk factor for AD. Glucose-dependent insulinotropic polypeptide (GIP) has been identified to be effective in T2DM treatment and neuroprotection. Objective: The present study investigated the neuroprotective effects and possible mechanisms of DAla2GIP-Glu-PAL, a novel long-lasting GIP analogue, in APP/PS1 AD mice. Methods: Multiple behavioral tests were performed to examine the cognitive function of mice. In vivo hippoca

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Silveyra, María-Ximena, Geneviève Evin, María-Fernanda Montenegro, et al. "Presenilin 1 Interacts with Acetylcholinesterase and Alters Its Enzymatic Activity and Glycosylation." Molecular and Cellular Biology 28, no. 9 (2008): 2908–19. http://dx.doi.org/10.1128/mcb.02065-07.

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ABSTRACT Presenilin 1 (PS1) plays a critical role in the γ-secretase processing of the amyloid precursor protein to generate the β-amyloid peptide, which accumulates in plaques in the pathogenesis of Alzheimer's disease (AD). Mutations in PS1 cause early onset AD, and proteins that interact with PS1 are of major functional importance. We report here the coimmunoprecipitation of PS1 and acetylcholinesterase (AChE), an enzyme associated with amyloid plaques. Binding occurs through PS1 N-terminal fragment independent of the peripheral binding site of AChE. Subcellular colocalization of PS1 and AC

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Sahu, Bijayani, Amy R. Mackos, Angela M. Floden, Loren E. Wold та Colin K. Combs. "Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice". Journal of Alzheimer's Disease 80, № 2 (2021): 761–74. http://dx.doi.org/10.3233/jad-200919.

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Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and neuronal death. There are several well-established genetic and environmental factors hypothesized to contribute to AD progression including air pollution. However, the molecular mechanisms by which air pollution exacerbates AD are unclear. Objective: This study explored the effects of particulate matter exposure on AD-related brain changes using the APP/PS1 transgenic model of disease. Methods: Male C57BL/6;C3H wild type and APP/PS

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Zoufal, Viktoria, Severin Mairinger, Markus Krohn, et al. "Measurement of cerebral ABCC1 transport activity in wild-type and APP/PS1-21 mice with positron emission tomography." Journal of Cerebral Blood Flow & Metabolism 40, no. 5 (2019): 954–65. http://dx.doi.org/10.1177/0271678x19854541.

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Previous data suggest a possible link between multidrug resistance-associated protein 1 (ABCC1) and brain clearance of beta-amyloid (Aβ). We used PET with 6-bromo-7-[11C]methylpurine ([11C]BMP) to measure cerebral ABCC1 transport activity in a beta-amyloidosis mouse model (APP/PS1-21) and in wild-type mice aged 50 and 170 days, without and with pretreatment with the ABCC1 inhibitor MK571. One hundred seventy days-old-animals additionally underwent [11C]PiB PET scans to measure Aβ load. While baseline [11C]BMP PET scans detected no differences in the elimination slope of radioactivity washout f

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Lu, Xin-Yi, Shun Huang, Qu-Bo Chen та ін. "Metformin Ameliorates Aβ Pathology by Insulin-Degrading Enzyme in a Transgenic Mouse Model of Alzheimer’s Disease". Oxidative Medicine and Cellular Longevity 2020 (21 квітня 2020): 1–10. http://dx.doi.org/10.1155/2020/2315106.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease. The accumulation of amyloid beta (Aβ) is the main pathology of AD. Metformin, a well-known antidiabetic drug, has been reported to have AD-protective effect. However, the mechanism is still unclear. In this study, we tried to figure out whether metformin could activate insulin-degrading enzyme (IDE) to ameliorate Aβ-induced pathology. Morris water maze and Y-maze results indicated that metformin could improve the learning and memory ability in APPswe/PS1dE9 (APP/PS1) transgenic mice. 18F-FDG PET-CT result showed that metfor

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Liu, Yao, Kelsey A. Hanson, Graeme McCormack, et al. "Enhanced Anti-Amyloid Effect of Combined Leptin and Pioglitazone in APP/PS1 Transgenic Mice." Current Alzheimer Research 17, no. 14 (2021): 1294–301. http://dx.doi.org/10.2174/1567205018666210218163857.

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Background: Alzheimer’s disease (AD) has challenged single-target therapeutic strategies, raising the possibility that combined therapies may offer a more effective treatment strategy. Objective: There is substantial evidence for the efficacy of leptin (L) (neuroprotective hormone) and pioglitazone (P) (anti-inflammatory agent) as monotherapies in AD. We have previously shown that combination treatment of L+P in APP/PS1 mice at the onset of pathology significantly improved memory and reduced brain Aβ levels relative to control mice. In this new study, we sought to replicate our previous findin

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Patel, Anant B., Vivek Tiwari, Pandichelvam Veeraiah та Kamal Saba. "Increased astroglial activity and reduced neuronal function across brain in AβPP-PS1 mouse model of Alzheimer’s disease". Journal of Cerebral Blood Flow & Metabolism 38, № 7 (2017): 1213–26. http://dx.doi.org/10.1177/0271678x17709463.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease associated with progressive loss of cognitive function, personality, and behavior. The present study evaluates neuronal and astroglial metabolic activity, and neurotransmitter cycle fluxes in AβPP-PS1 mouse model of AD by using 1H-[13C]-nuclear magnetic resonance (NMR) spectroscopy together with an infusion of either [1,6-13C2]glucose or [2-13C]acetate. The levels of N-acetyl-aspartate (NAA) and glutamate were found to be decreased in the cerebral cortex and hippocampus in AβPP-PS1 mice, when compared with wild type controls

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Handler, M., X. Yang, and J. Shen. "Presenilin-1 regulates neuronal differentiation during neurogenesis." Development 127, no. 12 (2000): 2593–606. http://dx.doi.org/10.1242/dev.127.12.2593.

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Mutations in Presenilin-1 (PS1) are a major cause of familial Alzheimer's disease. Our previous studies showed that PS1 is required for murine neural development. Here we report that lack of PS1 leads to premature differentiation of neural progenitor cells, indicating a role for PS1 in a cell fate decision between postmitotic neurons and neural progenitor cells. Neural proliferation and apoptotic cell death during neurogenesis are unaltered in PS1(−/−) mice, suggesting that the reduction in the neural progenitor cells observed in the PS1(−/−) brain is due to premature differentiation of progen

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Floden, Angela M., Mona Sohrabi, Suba Nookala, Jay J. Cao та Colin K. Combs. "Salivary Aβ Secretion and Altered Oral Microbiome in Mouse Models of AD". Current Alzheimer Research 17, № 12 (2021): 1133–44. http://dx.doi.org/10.2174/1567205018666210119151952.

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Background: Beta amyloid (Aβ) peptide containing plaque aggregations in the brain are a hallmark of Alzheimer’s Disease (AD). However, Aβ is produced by cell types outside of the brain suggesting that the peptide may serve a broad physiologic purpose. Objective: Based upon our prior work documenting expression of amyloid β precursor protein (APP) in intestinal epithelium we hypothesized that salivary epithelium might also express APP and be a source of Aβ. Methods: To begin testing this idea, we compared human age-matched control and AD salivary glands to C57BL/6 wild type, AppNL-G-F , and APP

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Zhang, Jiawei, Yaling Zheng, Yao Zhao, et al. "Andrographolide ameliorates neuroinflammation in APP/PS1 transgenic mice." International Immunopharmacology 96 (July 2021): 107808. http://dx.doi.org/10.1016/j.intimp.2021.107808.

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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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Xu, Yi-Jun, Yu Mei, Zi-Ling Qu, et al. "Ligustilide Ameliorates Memory Deficiency in APP/PS1 Transgenic Mice via Restoring Mitochondrial Dysfunction." BioMed Research International 2018 (July 10, 2018): 1–15. http://dx.doi.org/10.1155/2018/4606752.

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Ligustilide, the main lipophilic component of Radix angelicae sinensis, has been shown to ameliorate cognitive dysfunction in a few Alzheimer’s disease mouse models, but its mechanism is not fully understood. In this study, we employed 7-month-old APP/PS1 mice to explore whether LIG is able to protect against Alzheimer’s disease progression. The Morris water maze and Y-maze test results showed that eight weeks of intragastric administration of LIG (10 mg/kg, 40 mg/kg) every day improved memory deficit in APP/PS1 mice. The thioflavin-S staining and Western blot results (Aβ1-42monomer/oligomer,

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Wanek, Thomas, Viktoria Zoufal, Mirjam Brackhan, et al. "Brain Distribution of Dual ABCB1/ABCG2 Substrates Is Unaltered in a Beta-Amyloidosis Mouse Model." International Journal of Molecular Sciences 21, no. 21 (2020): 8245. http://dx.doi.org/10.3390/ijms21218245.

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Background: ABCB1 (P-glycoprotein) and ABCG2 (breast cancer resistance protein) are co-localized at the blood-brain barrier (BBB), where they restrict the brain distribution of many different drugs. Moreover, ABCB1 and possibly ABCG2 play a role in Alzheimer’s disease (AD) by mediating the brain clearance of beta-amyloid (Aβ) across the BBB. This study aimed to compare the abundance and activity of ABCG2 in a commonly used β-amyloidosis mouse model (APP/PS1-21) with age-matched wild-type mice. Methods: The abundance of ABCG2 was assessed by semi-quantitative immunohistochemical analysis of bra

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Pinçon, Anthony, Olivia De Montgolfier, Nilay Akkoyunlu, et al. "Non-Alcoholic Fatty Liver Disease, and the Underlying Altered Fatty Acid Metabolism, Reveals Brain Hypoperfusion and Contributes to the Cognitive Decline in APP/PS1 Mice." Metabolites 9, no. 5 (2019): 104. http://dx.doi.org/10.3390/metabo9050104.

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Non-alcoholic fatty liver disease (NAFLD), the leading cause of chronic liver disease, is associated with cognitive decline in middle-aged adults, but the mechanisms underlying this association are not clear. We hypothesized that NAFLD would unveil the appearance of brain hypoperfusion in association with altered plasma and brain lipid metabolism. To test our hypothesis, amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice were fed a standard diet or a high-fat, cholesterol and cholate diet, inducing NAFLD without obesity and hyperglycemia. The diet-induced NAFLD disturbed monounsa

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Jiménez-Palomares, Margarita, Juan José Ramos-Rodríguez, José Francisco López-Acosta та ін. "Increased Aβ production prompts the onset of glucose intolerance and insulin resistance". American Journal of Physiology-Endocrinology and Metabolism 302, № 11 (2012): E1373—E1380. http://dx.doi.org/10.1152/ajpendo.00500.2011.

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Type 2 diabetes (T2D) mellitus and Alzheimer's disease (AD) are two prevalent diseases with comparable pathophysiological features and genetic predisposition. Patients with AD are more susceptible to develop T2D. However, the molecular mechanism linking AD and T2D remains elusive. In this study, we have generated a new mouse model to test the hypothesis that AD would prompt the onset of T2D in mice. To test our hypothesis, we crossed Alzheimer APPswe/PS1dE9 (APP/PS1) transgenic mice with mice partially deficient in leptin signaling ( db/+). Body weight, plasma glucose, and insulin levels were

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Chen, Yijing, Lihua Fang, Shuo Chen, et al. "Gut Microbiome Alterations Precede Cerebral Amyloidosis and Microglial Pathology in a Mouse Model of Alzheimer’s Disease." BioMed Research International 2020 (May 27, 2020): 1–15. http://dx.doi.org/10.1155/2020/8456596.

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Emerging evidence suggests that the gut microbiome actively regulates cognitive functions and that gut microbiome imbalance is associated with Alzheimer’s disease (AD), the most prevalent neurodegenerative disorder. However, the changes in gut microbiome composition in AD and their association with disease pathology, especially in the early stages, are unclear. Here, we compared the profiles of gut microbiota between APP/PS1 transgenic mice (an AD mouse model) and their wild-type littermates at different ages by amplicon-based sequencing of 16S ribosomal RNA genes. Microbiota composition start

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Chi, Huimin, Qingfeng Zhai, Ming Zhang, et al. "APP/PS1 Gene-Environment Noise Interaction Aggravates AD-like Neuropathology in Hippocampus Via Activation of the VDAC1 Positive Feedback Loop." Current Alzheimer Research 18, no. 1 (2021): 14–24. http://dx.doi.org/10.2174/1567205018666210324114153.

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Background: Environmental risk factors, including environmental noise stress, and genetic factors, have been associated with the occurrence and development of Alzheimer’s disease (AD). However, the exact role and mechanism of AD-like pathology induced by environment-gene interactions between environmental noise and APP/PS1 gene remain elusive. Methods: Herein, we investigated the impact of chronic noise exposure on AD-like neuropathology in APP/PS1 transgenic mice. The Morris water maze (MWM) task was conducted to evaluate AD-like changes. The hippocampal phosphorylated Tau, amyloid-β (Aβ), an

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Vincent, Trevor J., Jonathan D. Thiessen, Laryssa M. Kurjewicz, et al. "Longitudinal Brain Size Measurements in App/Ps1 Transgenic Mice." Magnetic Resonance Insights 4 (January 2010): MRI.S5885. http://dx.doi.org/10.4137/mri.s5885.

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There appear to be species differences among the effects of gene mutations related to familial Alzheimer's disease on the brain during aging. To gain a better understanding of the effects of the Swedish mutation of amyloid precursor protein and the mutant form of human presenilin 1 on mice, commercially available mice from Jackson Laboratory were studied. Three dimensional T2*-weighted imaging was used to monitor the size of brains of APP/PS1 mice monthly, from 6 to 13 months of age. No significant difference was measured in the size of the medial-lateral width, dorsal-ventral height, rostral-

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Luo, Gang, Hongxia Xu, Yinuo Huang, et al. "Deposition of BACE-1 Protein in the Brains of APP/PS1 Double Transgenic Mice." BioMed Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/8380618.

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The main causes of Alzheimer’s disease remain elusive. Previous data have implicated the BACE-1 protein as a central player in the pathogenesis of Alzheimer’s disease. However, many inhibitors of BACE-1 have failed during preclinical and clinical trials for AD treatment. Therefore, uncovering the exact role of BACE-1 in AD may have significant impact on the future development of therapeutic agents. Three- and six-month-old female APP/PS1 double transgenic mice were used to study abnormal accumulation of BACE-1 protein in brains of mice here. Immunofluorescence, immunohistochemistry, and wester

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Cai, Zhiyou, Chuanling Wang, Wenbo He та Yi Chen. "Berberine Alleviates Amyloid-Beta Pathology in the Brain of APP/PS1 Transgenic Mice via Inhibiting β/γ-Secretases Activity and Enhancing α-Secretases". Current Alzheimer Research 15, № 11 (2018): 1045–52. http://dx.doi.org/10.2174/1567205015666180702105740.

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Background: Berberine (BBR) has neuroprotective effects on many brain diseases, including Alzheimer’s disease (AD). Amyloid -beta (Aβ) senile plaque is the most classical pathological hallmarks of AD. Aβ produces from a sequential cleavage by β-secretase (beta-site amyloid precursor protein cleaving enzyme 1, BACE1) and γ -secretase. The aim of our work was to investigate whether the neuroprotective effects of BBR on AD is related to inhibiting Aβ pathology. Method: The cognitive function of mice was assessed by the Morris water maze (MWM) test. The Aβ levels were determined by enzyme linked i

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Kim, Eunju, Kazunari Nohara, Marvin Wirianto, et al. "Effects of the Clock Modulator Nobiletin on Circadian Rhythms and Pathophysiology in Female Mice of an Alzheimer’s Disease Model." Biomolecules 11, no. 7 (2021): 1004. http://dx.doi.org/10.3390/biom11071004.

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Alzheimer’s disease (AD) is an age-related neurodegenerative disorder and the most common cause of dementia. Various pathogenic mechanisms have been proposed to contribute to disease progression, and recent research provided evidence linking dysregulated circadian rhythms/sleep and energy metabolism with AD. Previously, we found that the natural compound Nobiletin (NOB) can directly activate circadian cellular oscillators to promote metabolic health in disease models and healthy aging in naturally aged mice. In the current study, using the amyloid-β AD model APP/PS1, we investigated circadian,

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庄, 旭旭. "Research Progress of APP/PS1 Mice on Neuronal Apoptosis." Pharmacy Information 05, no. 02 (2016): 14–18. http://dx.doi.org/10.12677/pi.2016.52003.

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Bracko, Oliver, Brendah N. Njiru, Madisen Swallow, Muhammad Ali, Mohammad Haft-Javaherian, and Chris B. Schaffer. "Increasing cerebral blood flow improves cognition into late stages in Alzheimer’s disease mice." Journal of Cerebral Blood Flow & Metabolism 40, no. 7 (2019): 1441–52. http://dx.doi.org/10.1177/0271678x19873658.

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Alzheimer’s disease is associated with a 20–30% reduction in cerebral blood flow. In the APP/PS1 mouse model of Alzheimer’s disease, inhibiting neutrophil adhesion using an antibody against the neutrophil specific protein Ly6G was recently shown to drive rapid improvements in cerebral blood flow that was accompanied by an improvement in performance on short-term memory tasks. Here, in a longitudinal aging study, we assessed how far into disease development a single injection of anti-Ly6G treatment can acutely improve short-term memory function. We found that APP/PS1 mice as old as 15–16 months

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Wei, Xiaojie, Xiaohui Xu, Zhenfeng Chen, et al. "Protective Effects of 2-Dodecyl-6-Methoxycyclohexa-2,5 -Diene-1,4-Dione Isolated from Averrhoa Carambola L. (Oxalidaceae) Roots on Neuron Apoptosis and Memory Deficits in Alzheimer's Disease." Cellular Physiology and Biochemistry 49, no. 3 (2018): 1105–14. http://dx.doi.org/10.1159/000493289.

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Background/Aims: The roots of Averrhoa carambola L. (Oxalidaceae) have long been used as a traditional Chinese medicine for the treatment of headaches, vomiting, coughing and hangovers. 2-dodecyl-6-methoxycyclohexa-2, 5-1, 4-dione (DMDD) has been isolated from A. carambola L. roots, and this study was carried out to investigate the potential beneficial effects of DMDD on neuron apoptosis and memory deficits in Alzheimer's disease. Methods: The effects of a DMDD on learning and memory in APP/PS1 transgenic AD mice in vivo were investigated via Morris water maze and Y-type electric maze tests. I

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Garad, Machhindra, Elke Edelmann та Volkmar Leßmann. "Impairment of Spike-Timing-Dependent Plasticity at Schaffer Collateral-CA1 Synapses in Adult APP/PS1 Mice Depends on Proximity of Aβ Plaques". International Journal of Molecular Sciences 22, № 3 (2021): 1378. http://dx.doi.org/10.3390/ijms22031378.

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Alzheimer’s disease (AD) is a multifaceted neurodegenerative disorder characterized by progressive and irreversible cognitive decline, with no disease-modifying therapy until today. Spike timing-dependent plasticity (STDP) is a Hebbian form of synaptic plasticity, and a strong candidate to underlie learning and memory at the single neuron level. Although several studies reported impaired long-term potentiation (LTP) in the hippocampus in AD mouse models, the impact of amyloid-β (Aβ) pathology on STDP in the hippocampus is not known. Using whole cell patch clamp recordings in CA1 pyramidal neur

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Cong, Wei-hong, Bin Yang, Li Xu та ін. "Herbal Extracts Combination (WNK) Prevents Decline in Spatial Learning and Memory in APP/PS1 Mice through Improvement of Hippocampal AβPlaque Formation, Histopathology, and Ultrastructure". Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/478190.

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To investigate the cognitive enhancement effect of WNK, an extracts combination ofP. ginseng, G. biloba, andC. sativusL. and possible mechanisms, 5-month-old APP/PS1 transgenic mice were used in this study. After 3 months of administration, all mice received Morris water maze (MWM) training and a probe test. Mouse brain sections were detected by immunohistochemistry, HE staining, and transmission electron microscopy. MWM results showed significant difference between transgenic mice and nontransgenic littermates (P<0.05,P<0.01). WNK-treated mice exhibited enhanced maze performance over th

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Hou, Yujun, Yong Wei, Sofie Lautrup, et al. "NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer’s disease via cGAS–STING." Proceedings of the National Academy of Sciences 118, no. 37 (2021): e2011226118. http://dx.doi.org/10.1073/pnas.2011226118.

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Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disorder. Impaired neuronal bioenergetics and neuroinflammation are thought to play key roles in the progression of AD, but their interplay is not clear. Nicotinamide adenine dinucleotide (NAD+) is an important metabolite in all human cells in which it is pivotal for multiple processes including DNA repair and mitophagy, both of which are impaired in AD neurons. Here, we report that levels of NAD+ are reduced and markers of inflammation increased in the brains of APP/PS1 mutant transgenic mice with beta-amyloid pathology. Tr

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Han, Hui, Feng Wang, Juanjuan Chen, et al. "Changes in Biothiol Levels Are Closely Associated with Alzheimer’s Disease." Journal of Alzheimer's Disease 82, no. 2 (2021): 527–40. http://dx.doi.org/10.3233/jad-210021.

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Background: Serum homocysteine (Hcy) level is considered to be an important biomarker for Alzheimer’s disease (AD); however, the status of Hcy in brain tissue, and the association between brain and serum levels of Hcy in AD patients remain unclear. Objective: We aimed to examine whether the changes of three thiols are consistent in serum of AD patients and the brain of APP/PS1 mice, and to verify the effectiveness of Hcy as a biomarker for early AD detection. Methods: The levels of Hcy, cysteine (Cys), and glutathione (GSH) in Aβ1–42-treated PC12 cells, the brain and hippocampus of APP/PS1 mou

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Leissring, Malcolm A., Yama Akbari, Christopher M. Fanger, Michael D. Cahalan, Mark P. Mattson, and Frank M. LaFerla. "Capacitative Calcium Entry Deficits and Elevated Luminal Calcium Content in Mutant Presenilin-1 Knockin Mice." Journal of Cell Biology 149, no. 4 (2000): 793–98. http://dx.doi.org/10.1083/jcb.149.4.793.

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Dysregulation of calcium signaling has been causally implicated in brain aging and Alzheimer's disease. Mutations in the presenilin genes (PS1, PS2), the leading cause of autosomal dominant familial Alzheimer's disease (FAD), cause highly specific alterations in intracellular calcium signaling pathways that may contribute to the neurodegenerative and pathological lesions of the disease. To elucidate the cellular mechanisms underlying these disturbances, we studied calcium signaling in fibroblasts isolated from mutant PS1 knockin mice. Mutant PS1 knockin cells exhibited a marked potentiation in

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Wilson, Christina A., Diane D. Murphy, Benoit I. Giasson, Bin Zhang, John Q. Trojanowski та Virginia M. Y. Lee. "Degradative organelles containing mislocalized α- and β-synuclein proliferate in presenilin-1 null neurons". Journal of Cell Biology 165, № 3 (2004): 335–46. http://dx.doi.org/10.1083/jcb.200403061.

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Presenilin-1 null mutation (PS1 −/−) in mice is associated with morphological alterations and defects in cleavage of transmembrane proteins. Here, we demonstrate that PS1 deficiency also leads to the formation of degradative vacuoles and to the aberrant translocation of presynaptic α- and β-synuclein proteins to these organelles in the perikarya of primary neurons, concomitant with significant increases in the levels of both synucleins. Stimulation of autophagy in control neurons produced a similar mislocalization of synucleins as genetic ablation of PS1. These effects were not the result of t

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Liu, Meixia, Yun Wei, Yang Yang, et al. "Effects and Mechanism of Huannao Yicong Decoction Extract on the Ethology of Transgenic APP/PS1 Mice." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/9502067.

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To investigate the mechanism of Huannao Yicong Decoction (HYD) extract on improving of learning memory of transgenic amyloid precursor protein (APP)/presenilin 1 (PS1) mice, we randomly divided 60 transgenic APP/PS1 mice of 3 months old into 4 groups: the model group, the Donepezil group, the HYD-L group, and the HYD-H group, with 15 C57BL/6J mice of the same genetic background as the control group. These mice were gavaged for 6 months in a row. The results showed that the latency was significantly shortened and the number of passing through the original platform was increased. HYD extract can

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Sun, Xiao-Lei, Jia-Bao Zhang, Yun-Xiang Guo та ін. "Xanthohumol ameliorates memory impairment and reduces the deposition of β-amyloid in APP/PS1 mice via regulating the mTOR/LC3II and Bax/Bcl-2 signalling pathways". Journal of Pharmacy and Pharmacology 73, № 9 (2021): 1230–39. http://dx.doi.org/10.1093/jpp/rgab052.

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Abstract Objectives Xanthohumol (XAN) is a unique component of Humulus lupulus L. and is known for its diverse biological activities. In this study, we investigated whether Xanthohumol could ameliorate memory impairment of APP/PS1 mice, and explored its potential mechanism of action. Methods APP/PS1 mice were used for in vivo test and were treated with N-acetylcysteine and Xanthohumol for 2 months. Learning and memory levels were evaluated by the Morris water maze. Inflammatory and oxidative markers in serum and hippocampus and the deposition of Aβ in the hippocampus were determined. Moreover,

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López-González, Irene, Agatha Schlüter, Ester Aso, et al. "Neuroinflammatory Signals in Alzheimer Disease and APP/PS1 Transgenic Mice." Journal of Neuropathology & Experimental Neurology 74, no. 4 (2015): 319–44. http://dx.doi.org/10.1097/nen.0000000000000176.

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Du, Jing, Yu Liang, Feng Xu, Bing Sun, and Zhao Wang. "Trehalose rescues Alzheimer's disease phenotypes in APP/PS1 transgenic mice." Journal of Pharmacy and Pharmacology 65, no. 12 (2013): 1753–56. http://dx.doi.org/10.1111/jphp.12108.

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Kraft, Andrew W., Xiaoyan Hu, Hyejin Yoon, et al. "Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice." FASEB Journal 27, no. 1 (2012): 187–98. http://dx.doi.org/10.1096/fj.12-208660.

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Bao, Jian, Wei Liu, Hong-yan Zhou, et al. "Epigallocatechin-3-gallate Alleviates Cognitive Deficits in APP/PS1 Mice." Current Medical Science 40, no. 1 (2020): 18–27. http://dx.doi.org/10.1007/s11596-020-2142-z.

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Caccamo, Antonella, Caterina Branca, Eric Ferreira, and Salvatore Oddo. "[P2-156]: INCREASED SUSCEPTIBILITY TO NECROPTOSIS IN APP/PS1 MICE." Alzheimer's & Dementia 13, no. 7S_Part_13 (2017): P667. http://dx.doi.org/10.1016/j.jalz.2017.06.807.

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Martín-Belmonte, Alejandro, Carolina Aguado, Rocío Alfaro-Ruiz, et al. "The Density of Group I mGlu5 Receptors Is Reduced along the Neuronal Surface of Hippocampal Cells in a Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 22, no. 11 (2021): 5867. http://dx.doi.org/10.3390/ijms22115867.

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Metabotropic glutamate receptor subtype 5 (mGlu5) is implicated in the pathophysiology of Alzheimer’s disease (AD). However, its alteration at the subcellular level in neurons is still unexplored. Here, we provide a quantitative description on the expression and localisation patterns of mGlu5 in the APP/PS1 model of AD at 12 months of age, combining immunoblots, histoblots and high-resolution immunoelectron microscopic approaches. Immunoblots revealed that the total amount of mGlu5 protein in the hippocampus, in addition to downstream molecules, i.e., Gq/11 and PLCβ1, was similar in both APP/P

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Takkinen, Jatta S., Francisco R. López-Picón, Rana Al Majidi, et al. "Brain energy metabolism and neuroinflammation in ageing APP/PS1-21 mice using longitudinal 18F-FDG and 18F-DPA-714 PET imaging." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (2016): 2870–82. http://dx.doi.org/10.1177/0271678x16677990.

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Preclinical animal model studies of brain energy metabolism and neuroinflammation in Alzheimer’s disease have produced conflicting results, hampering both the elucidation of the underlying disease mechanism and the development of effective Alzheimer’s disease therapies. Here, we aimed to quantify the relationship between brain energy metabolism and neuroinflammation in the APP/PS1-21 transgenic mouse model of Alzheimer’s disease using longitudinal in vivo18F-FDG and 18F-DPA-714) PET imaging and ex vivo brain autoradiography. APP/PS1-21 (TG, n = 9) and wild type control mice (WT, n = 9) were st

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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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Lonnemann, Niklas, Shirin Hosseini, Carlo Marchetti, et al. "The NLRP3 inflammasome inhibitor OLT1177 rescues cognitive impairment in a mouse model of Alzheimer’s disease." Proceedings of the National Academy of Sciences 117, no. 50 (2020): 32145–54. http://dx.doi.org/10.1073/pnas.2009680117.

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Numerous studies demonstrate that neuroinflammation is a key player in the progression of Alzheimer’s disease (AD). Interleukin (IL)-1β is a main inducer of inflammation and therefore a prime target for therapeutic options. The inactive IL-1β precursor requires processing by the the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome into a mature and active form. Studies have shown that IL-1β is up-regulated in brains of patients with AD, and that genetic inactivation of the NLRP3 inflammasome improves behavioral tests and synaptic pl

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