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Artykuły w czasopismach na temat „3xtg-AD”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 21 lutego 2023

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1

Al-Nakkash, Layla, Daniel Mason, Niamatullah Ismail, et al. "Exercise Training Prevents the Loss of Wall Thickness and Lowers Expression of Alzheimer’s Related Proteins in 3xTg Mouse Jejunum." International Journal of Environmental Research and Public Health 19, no. 21 (2022): 14164. http://dx.doi.org/10.3390/ijerph192114164.

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Growing evidence has demonstrated the benefits of regular exercise on cardiovascular, neural, and cognitive function in humans with Alzheimer’s disease (AD). However, the consequences of AD on gastrointestinal morphology and the effects of regular exercise, which plays an important role against the development of certain gastrointestinal-related diseases, are still poorly understood. Therefore, to assess the changes in intestinal structure in a mouse model of AD and the impact of exercise, 2-month-old 3xTg-AD male mice were subjected to treadmill running 5 days per week for a period of 5 month

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Cross, Donna J., Bertrand R. Huber, Michael A. Silverman, et al. "Intranasal Paclitaxel Alters Alzheimer’s Disease Phenotypic Features in 3xTg-AD Mice." Journal of Alzheimer's Disease 83, no. 1 (2021): 379–94. http://dx.doi.org/10.3233/jad-210109.

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Background: Microtubule stabilizing drugs, commonly used as anti-cancer therapeutics, have been proposed for treatment of Alzheimer’s disease (AD); however, many do not cross the blood-brain barrier. Objective: This research investigated if paclitaxel (PTX) delivered via the intranasal (IN) route could alter the phenotypic progression of AD in 3xTg-AD mice. Methods: We administered intranasal PTX in 3XTg-AD mice (3xTg-AD n = 15, 10 weeks and n = 10, 44 weeks, PTX: 0.6 mg/kg or 0.9%saline (SAL)) at 2-week intervals. After treatment, 3XTg-AD mice underwent manganese-enhanced magnetic resonance i

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Várkonyi, Dorottya, Bibiána Török, Eszter Sipos, et al. "Investigation of Anxiety- and Depressive-like Symptoms in 4- and 8-Month-Old Male Triple Transgenic Mouse Models of Alzheimer’s Disease." International Journal of Molecular Sciences 23, no. 18 (2022): 10816. http://dx.doi.org/10.3390/ijms231810816.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. Approximately 50% of AD patients show anxiety and depressive symptoms, which may contribute to cognitive decline. We aimed to investigate whether the triple-transgenic mouse (3xTg-AD) is a good preclinical model of this co-morbidity. The characteristic histological hallmarks are known to appear around 6-month; thus, 4- and 8-month-old male mice were compared with age-matched controls. A behavioral test battery was used to examine anxiety- (open field (OF), elevated plus maze, light-dark b

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4

Magri, Chiara, Erika Vitali, Sara Cocco, et al. "Whole Blood Transcriptome Characterization of 3xTg-AD Mouse and Its Modulation by Transcranial Direct Current Stimulation (tDCS)." International Journal of Molecular Sciences 22, no. 14 (2021): 7629. http://dx.doi.org/10.3390/ijms22147629.

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The 3xTg-AD mouse is a widely used model in the study of Alzheimer’s Disease (AD). It has been extensively characterized from both the anatomical and behavioral point of view, but poorly studied at the transcriptomic level. For the first time, we characterize the whole blood transcriptome of the 3xTg-AD mouse at three and six months of age and evaluate how its gene expression is modulated by transcranial direct current stimulation (tDCS). RNA-seq analysis revealed 183 differentially expressed genes (DEGs) that represent a direct signature of the genetic background of the mouse. Moreover, in th

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Yan, Xu-Dong, Xue-Song Qu, Jing Yin, et al. "Adiponectin Ameliorates Cognitive Behaviors and in vivo Synaptic Plasticity Impairments in 3xTg-AD Mice." Journal of Alzheimer's Disease 85, no. 1 (2022): 343–57. http://dx.doi.org/10.3233/jad-215063.

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Background: Cognitive deficit is mainly clinical characteristic of Alzheimer’s disease (AD). Recent reports showed adiponectin and its analogues could reverse cognitive impairments, lower amyloid-β protein (Aβ) deposition, and exert anti-inflammatory effects in different APP/PS1 AD model mice mainly exhibiting amyloid plaque pathology. However, the potential in vivo electrophysiological mechanism of adiponectin protecting against cognitive deficits in AD and the neuroprotective effects of adiponectin on 3xTg-AD mice including both plaque and tangle pathology are still unclear. Objective: To ob

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Roda, Alejandro R., Laia Montoliu-Gaya, Gabriel Serra-Mir та Sandra Villegas. "Both Amyloid-β Peptide and Tau Protein Are Affected by an Anti-Amyloid-β Antibody Fragment in Elderly 3xTg-AD Mice". International Journal of Molecular Sciences 21, № 18 (2020): 6630. http://dx.doi.org/10.3390/ijms21186630.

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Alzheimer’s disease (AD) is the most common dementia worldwide. According to the amyloid hypothesis, the early accumulation of the Aβ-peptide triggers tau phosphorylation, synaptic dysfunction, and eventually neuronal death leading to cognitive impairment, as well as behavioral and psychological symptoms of dementia. ScFv-h3D6 is a single-chain variable fragment that has already shown its ability to diminish the amyloid burden in 5-month-old 3xTg-AD mice. However, tau pathology is not evident at this early stage of the disease in this mouse model. In this study, the effects of scFv-h3D6 on Aβ

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Tan, Chenxi, Yang Liu, Huiyi Zhang, et al. "Neuroprotective Effects of Probiotic-Supplemented Diet on Cognitive Behavior of 3xTg-AD Mice." Journal of Healthcare Engineering 2022 (January 5, 2022): 1–10. http://dx.doi.org/10.1155/2022/4602428.

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Alzheimer’s disease (AD) is recognized as one of the most common types of senile dementia. AD patients first suffer memory loss for recent events (short-term memory impairment). As the disease progresses, they are deprived of self-awareness. This study aims to explore the effects of a probiotic-supplemented diet on the cognitive behaviors and pathological features of mouse models of Alzheimer’s disease (AD). Mice in the control group and the 3xTg-AD group were fed a regular diet and a probiotic-supplemented diet, respectively, for 20 weeks. Behavioral experiments like Morris’s water maze and Y

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Nie, Lulin, Junxia Xia, Honglian Li, et al. "Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–17. http://dx.doi.org/10.1155/2017/6473506.

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Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Pr

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9

Kim, Juyong, Siyoung Lee, Jaekyoon Kim та ін. "Ca2+-permeable TRPV1 pain receptor knockout rescues memory deficits and reduces amyloid-β and tau in a mouse model of Alzheimer’s disease". Human Molecular Genetics 29, № 2 (2019): 228–37. http://dx.doi.org/10.1093/hmg/ddz276.

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Abstract The transient receptor potential vanilloid 1 (TRPV1) protein is a pain receptor that elicits a hot sensation when an organism eats the capsaicin of red chili peppers. This calcium (Ca2+)-permeable cation channel is mostly expressed in the peripheral nervous system sensory neurons but also in the central nervous system (e.g. hippocampus and cortex). Preclinical studies found that TRPV1 mediates behaviors associated with anxiety and depression. Loss of TRPV1 functionality increases expression of genes related to synaptic plasticity and neurogenesis. Thus, we hypothesized that TRPV1 defi

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Oh, Kwang-Jin, Sylvia E. Perez, Sarita Lagalwar, Laurel Vana, Lester Binder, and Elliott J. Mufson. "Staging of Alzheimer's Pathology in Triple Transgenic Mice: A Light and Electron Microscopic Analysis." International Journal of Alzheimer's Disease 2010 (2010): 1–24. http://dx.doi.org/10.4061/2010/780102.

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The age-related pathological cascade underlying intraneuronal tau formation in 3xTg-AD mice, which harbor the humanAPPSwe,PS1M126V, andTauP301Lgene mutations, remains unclear. At 3 weeks of age, AT180, Alz50, MC1, AT8, and PHF-1 intraneuronal immunoreactivity appeared in the amygdala and hippocampus and at later ages in the cortex of 3xTg-AD mice. AT8 and PHF-1 staining was fixation dependent in young mutant mice. 6E10 staining was seen at all ages. Fluorescent immunomicroscopy revealed CA1 neurons dual stained for 6E10 and Alz50 and single Alz50 immunoreactive neurons in the subiculum at 3 we

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11

Su, Cen, Ping Niu, Yao-ming Xu, Ye Feng, and Hai-ping Xia. "Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice." Tropical Journal of Pharmaceutical Research 18, no. 9 (2021): 1903–7. http://dx.doi.org/10.4314/tjpr.v18i9.17.

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Purpose: To investigate the protective effect of Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice. Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the

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Jullienne, Amandine, Ryan Quan, Jenny I. Szu, Michelle V. Trinh, Erik J. Behringer, and Andre Obenaus. "Progressive Vascular Abnormalities in the Aging 3xTg-AD Mouse Model of Alzheimer’s Disease." Biomedicines 10, no. 8 (2022): 1967. http://dx.doi.org/10.3390/biomedicines10081967.

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Vascular dysfunction and structural abnormalities in Alzheimer’s disease (AD) are known to contribute to the progression of the pathology, and studies have tended to ignore the role of the vasculature in AD progression. We utilized the 3xTg-AD mouse model of AD to examine individual cerebral vessels and the cortical vascular network across the lifespan. Our vessel painting approach was used to label the entire cortical vasculature, followed by epifluorescence microscopy. The middle cerebral artery (MCA) tree was assessed with confocal microscopy, and a new method was developed to assess branch

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Ma, Donglai, Wei Song, Minesh Kapadia, Margaret Fahnestock, and Boris Sakic. "Age-Dependent Synthesis of Diverse Autoantibodies in the 3xTg-AD Model of Alzheimer’s Disease." Journal of Immunology 204, no. 1_Supplement (2020): 64.5. http://dx.doi.org/10.4049/jimmunol.204.supp.64.5.

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Abstract Elevated levels of serum autoantibodies are a well-documented phenomenon in patients with Alzheimer’s disease (AD), but the nature of the autoimmunity is unclear. Triple-transgenic (3xTg-AD) mice are a well-established model that develops AD-like pathology. We observed that recent cohorts of male 3xTg-AD mice exhibit autoimmune manifestations, yet lack plaque/tangle pathology. In the current study, we identified the time course and type of autoantibodies produced during the progression and attenuation of systemic autoimmunity. Tissue samples were collected from 3xTg-AD and wild type (

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Bae, Hyunsu, Hyunjung Baek, Minsook Ye, et al. "Neuromodulatory activities of CD4+CD25+Foxp3+ regulatory T cells in 3xTg-AD Alzheimer’s disease model." Journal of Immunology 196, no. 1_Supplement (2016): 214.1. http://dx.doi.org/10.4049/jimmunol.196.supp.214.1.

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Abstract Alzheimer’s disease (AD) is the most prevalent cause of dementia marked by progressive cognitive and functional impairment and memory loss. AD patients display neuropathological lesions including deposition of extracellular amyloid-beta (Aβ) peptide and the formation of neurofibrillary tangles. Although the mechanisms causing brain atrophy and neuronal death are largely unknown, increasing evidence suggests that immunity plays a critical role in the pathogenesis of AD. In the present study, we investigated the effect of regulatory T cells (Tregs) on AD mouse model. First, we transient

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Dennison, Jessica L., Natalie R. Ricciardi, Ines Lohse, Claude-Henry Volmar, and Claes Wahlestedt. "Sexual Dimorphism in the 3xTg-AD Mouse Model and Its Impact on Pre-Clinical Research." Journal of Alzheimer's Disease 80, no. 1 (2021): 41–52. http://dx.doi.org/10.3233/jad-201014.

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Female sex is a leading risk factor for developing Alzheimer’s disease (AD). Sexual dimorphism in AD is gaining attention as clinical data show that women are not only more likely to develop AD but also to experience worse pathology and faster cognitive decline. Pre-clinical AD research in animal models often neglects to address sexual dimorphism in evaluation of behavioral or molecular characteristics and outcomes. This can compromise its translation to a clinical setting. The triple-transgenic AD mouse model (3xTg-AD) is a commonly used but unique AD model because it exhibits both amyloid an

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Stojakovic, Andrea, Su-Youne Chang, Jarred Nesbitt, et al. "Partial Inhibition of Mitochondrial Complex I Reduces Tau Pathology and Improves Energy Homeostasis and Synaptic Function in 3xTg-AD Mice." Journal of Alzheimer's Disease 79, no. 1 (2021): 335–53. http://dx.doi.org/10.3233/jad-201015.

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Background: Accumulation of hyperphosphorylated tau (pTau) protein is associated with synaptic dysfunction in Alzheimer’s disease (AD). We previously demonstrated that neuroprotection in familial mouse models of AD could be achieved by targeting mitochondria complex I (MCI) and activating the adaptive stress response. Efficacy of this strategy on pTau-related pathology remained unknown. Objective: To investigate the effect of specific MCI inhibitor tricyclic pyrone compound CP2 on levels of human pTau, memory function, long term potentiation (LTP), and energy homeostasis in 18-month-old 3xTg-A

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Ruffinatti, F., L. Tapella, I. Gregnanin, et al. "Transcriptional Remodeling in Primary Hippocampal Astrocytes from an Alzheimer’s Disease Mouse Model." Current Alzheimer Research 15, no. 11 (2018): 986–1004. http://dx.doi.org/10.2174/1567205015666180613113924.

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Background: It is well known that alterations in astrocytes occur in Alzheimer’s disease and reactive astrogliosis is one of the hallmarks of the disease. Recently, data has emerged that suggests that alterations in astrocytes may also occur early in the pathogenesis of the disease. Objective: The aim of present work was to characterize the transcriptional alterations occurring in cultured astrocytes from 3xTg-AD mouse pups compared to control non-transgenic mice. Furthermore, we also compared these changes to those reported by others in astrocytes from symptomatic AD mice. Method: We conducte

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Cai, Ang, Liu Xiao, Yan-Ping Zhou, Zhi-Guo Zhang, and Quan-Wei Yang. "Effect of Evodia rutaecarpa (Juss) Benth extract on Alzheimer disease in mice." Tropical Journal of Pharmaceutical Research 19, no. 4 (2020): 823–28. http://dx.doi.org/10.4314/tjpr.v19i4.21.

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Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spe

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Escrig, Anna, Amalia Molinero, Brenda Méndez, et al. "IL-6 Trans-Signaling in the Brain Influences the Metabolic Phenotype of the 3xTg-AD Mouse Model of Alzheimer’s Disease." Cells 9, no. 7 (2020): 1605. http://dx.doi.org/10.3390/cells9071605.

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Alzheimer’s disease (AD) is a neurodegenerative disorder that causes the most prevalent dementia in the elderly people. Obesity and insulin resistance, which may cause major health problems per se, are risk factors for AD, and cytokines such as interleukin-6 (IL-6) have a role in these conditions. IL-6 can signal either through a membrane receptor or by trans-signaling, which can be inhibited by the soluble form of the co-receptor gp130 (sgp130). We have addressed the possibility that blocking IL-6 trans-signaling in the brain could have an effect in the triple transgenic 3xTg-AD mouse model o

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Giovinazzo, Daniel, Biljana Bursac, Juan I. Sbodio та ін. "Hydrogen sulfide is neuroprotective in Alzheimer’s disease by sulfhydrating GSK3β and inhibiting Tau hyperphosphorylation". Proceedings of the National Academy of Sciences 118, № 4 (2021): e2017225118. http://dx.doi.org/10.1073/pnas.2017225118.

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Alzheimer’s disease (AD), the most common cause of dementia and neurodegeneration in the elderly, is characterized by deterioration of memory and executive and motor functions. Neuropathologic hallmarks of AD include neurofibrillary tangles (NFTs), paired helical filaments, and amyloid plaques. Mutations in the microtubule-associated protein Tau, a major component of the NFTs, cause its hyperphosphorylation in AD. We have shown that signaling by the gaseous molecule hydrogen sulfide (H2S) is dysregulated during aging. H2S signals via a posttranslational modification termed sulfhydration/persul

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Bae, Hyunsu, Minsook Ye, Chanju Lee, Hwan-Suck Chung, and Insop Shim. "Neuroprotective effects of bee venom phospholipase A2 mediated by the suppression of neuroinflammatory responses in the 3xTg AD mouse model of Alzheimer’s disease (THER2P.967)." Journal of Immunology 194, no. 1_Supplement (2015): 67.18. http://dx.doi.org/10.4049/jimmunol.194.supp.67.18.

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Abstract Alzheimer’s disease (AD) is a severe neuroinflammatory disease. CD4+Foxp3+ regulatory T cells (Tregs) play a pivotal role in maintaining immune tolerance in various inflammatory diseases. In this study, we sought to determine whether bee venom PLA2 promotes cognitive function in and modulates the patho-immunological features of AD in 3xTg-AD mice. PLA2 treatment significantly enhanced the cognitive function of the 3xTg-AD mice and increased glucose metabolism, as assessed with 18F-2 fluoro-2-deoxy-D-glucose ([F-18] FDG) positron emission tomography (PET). The levels of amyloid beta (A

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Manna, Jayeeta, Gary L. Dunbar, and Panchanan Maiti. "Curcugreen Treatment Prevented Splenomegaly and Other Peripheral Organ Abnormalities in 3xTg and 5xFAD Mouse Models of Alzheimer’s Disease." Antioxidants 10, no. 6 (2021): 899. http://dx.doi.org/10.3390/antiox10060899.

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Metabolic dysfunction and immune disorders are common in Alzheimer’s disease (AD). The mechanistic details of these epiphenomena in AD are unclear. Here, we have investigated whether a highly bioavailable curcuminoid formulation, curcugreen (CGR), can prevent abnormalities in peripheral organs of two mouse models of AD. Eighteen- and 24-month-old male and female 3xTg and 5xFAD mice were treated with CGR (100 mg/kg) for 2 months, orally. Cytoarchitectural changes of spleen, liver, kidney and lungs were studied by H&E stain. Apoptotic death was confirmed by TUNEL staining. Amyloid deposition

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Roda, Alejandro R., Gisela Esquerda-Canals, Joaquim Martí-Clúa та Sandra Villegas. "Cognitive Impairment in the 3xTg-AD Mouse Model of Alzheimer’s Disease is Affected by Aβ-ImmunoTherapy and Cognitive Stimulation". Pharmaceutics 12, № 10 (2020): 944. http://dx.doi.org/10.3390/pharmaceutics12100944.

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Clinical symptoms of Alzheimer’s Disease (AD) include behavioral alterations and cognitive impairment. These functional phenotypes early occur in triple-transgenic (3xTg-AD) mice. Specifically, behavioral alterations are first detected when mice are at around 2.5 months old and cognitive impairment in between 3- and 5-month-old mice. In this work, the effect of chronic Aβ-immunotherapy on behavioral and cognitive abilities was tested by monthly administering the antibody fragment scFv-h3D6 to 3xTg-AD female mice from 5 to 9 months of age. An untreated group was used as a reference, as well as

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Martínez-Iglesias, Olaia, Vinogran Naidoo, Iván Carrera, and Ramón Cacabelos. "Epigenetic Studies in the Male APP/BIN1/COPS5 Triple-Transgenic Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 23, no. 5 (2022): 2446. http://dx.doi.org/10.3390/ijms23052446.

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Alzheimer’s Disease (AD) is a major health problem worldwide. The lack of efficacy of existing therapies for AD is because of diagnosis at late stages of the disease, limited knowledge of biomarkers, and molecular mechanisms of AD pathology, as well as conventional drugs that are focused on symptomatic rather than mechanistic features of the disease. The connection between epigenetics and AD, however, may be useful for the development of novel therapeutics or diagnostic biomarkers for AD. The aim of this study was to investigate a pathogenic role for epigenetics and other biomarkers in the mal

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Muntsant, Aida, Francesc Jiménez-Altayó, Lidia Puertas-Umbert, Elena Jiménez-Xarrie, Elisabet Vila, and Lydia Giménez-Llort. "Sex-Dependent End-of-Life Mental and Vascular Scenarios for Compensatory Mechanisms in Mice with Normal and AD-Neurodegenerative Aging." Biomedicines 9, no. 2 (2021): 111. http://dx.doi.org/10.3390/biomedicines9020111.

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Life expectancy decreases with aging, with cardiovascular, mental health, and neurodegenerative disorders strongly contributing to the total disability-adjusted life years. Interestingly, the morbidity/mortality paradox points to females having a worse healthy life expectancy. Since bidirectional interactions between cardiovascular and Alzheimer’s diseases (AD) have been reported, the study of this emerging field is promising. In the present work, we further explored the cardiovascular–brain interactions in mice survivors of two cohorts of non-transgenic and 3xTg-AD mice, including both sexes,

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Szabó, Adrienn, Szidónia Farkas, Csilla Fazekas, et al. "Temporal Appearance of Enhanced Innate Anxiety in Alzheimer Model Mice." Biomedicines 11, no. 2 (2023): 262. http://dx.doi.org/10.3390/biomedicines11020262.

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The prevalence of Alzheimer’s disorder (AD) is increasing worldwide, and the co-morbid anxiety is an important, albeit often neglected problem, which might appear early during disease development. Animal models can be used to study this question. Mice, as prey animals, show an innate defensive response against a predator odor, providing a valuable tool for anxiety research. Our aim was to test whether the triple-transgenic mice model of AD shows signs of innate anxiety, with specific focus on the temporal appearance of the symptoms. We compared 3xTg-AD mice bearing human mutations of amyloid p

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Djordjevic, Jelena, Subir Roy Chowdhury, Wanda M. Snow, et al. "Early Onset of Sex-Dependent Mitochondrial Deficits in the Cortex of 3xTg Alzheimer’s Mice." Cells 9, no. 6 (2020): 1541. http://dx.doi.org/10.3390/cells9061541.

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Alzheimer’s disease (AD) is a major public health concern worldwide. Advanced age and female sex are two of the most prominent risk factors for AD. AD is characterized by progressive neuronal loss, especially in the cortex and hippocampus, and mitochondrial dysfunction has been proposed to be an early event in the onset and progression of the disease. Our results showed early perturbations in mitochondrial function in 3xTg mouse brain, with the cortex being more susceptible to mitochondrial changes than the hippocampus. In the cortex of 3xTg females, decreased coupled and uncoupled respiration

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Salobrar-García, Elena, Ana C. Rodrigues-Neves, Ana I. Ramírez, et al. "Microglial Activation in the Retina of a Triple-Transgenic Alzheimer’s Disease Mouse Model (3xTg-AD)." International Journal of Molecular Sciences 21, no. 3 (2020): 816. http://dx.doi.org/10.3390/ijms21030816.

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Alzheimer’s disease (AD) is the most common type of dementia in the world. The main biomarkers associated with AD are protein amyloid-β (Aβ) plaques and protein tau neurofibrillary tangles, which are responsible for brain neuroinflammation mediated by microglial cells. Increasing evidence has shown that the retina can also be affected in AD, presenting some molecular and cellular changes in the brain, such as microglia activation. However, there are only a few studies assessing such changes in the retinal microglia in animal models of AD. These studies use retinal sections, which have some lim

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Marín-Pardo, Daniela, and Lydia Gimenez-Llort. "417 - Olfactory signatures in models of aging and Alzheimer’s disease and the effect of social isolation: A translational neuroscience approach in times of coronavirus pandemic (COVID-19)." International Psychogeriatrics 32, S1 (2020): 133. http://dx.doi.org/10.1017/s1041610220002707.

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Sensory systems ensure the ability to perceive and recognize the world. Therefore, the temporal course and the severity of their involution through the aging process can be critical. In the elderly, sensory impairments significantly increase their risk of biological, psychological and social impoverishment. Olfactory loss, known to happen in bacterial and viral infections and considered an early biomarker in Alzheimer’s and Parkinson’s diseases neurodegenerative processes, has been reported also as an early indicator of current infection by SARS-CoV-2. At the translational level, in the presen

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Castillo-Mariqueo, Lidia, M. José Pérez-García, and Lydia Giménez-Llort. "Modeling Functional Limitations, Gait Impairments, and Muscle Pathology in Alzheimer’s Disease: Studies in the 3xTg-AD Mice." Biomedicines 9, no. 10 (2021): 1365. http://dx.doi.org/10.3390/biomedicines9101365.

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Gait impairments in Alzheimer’s disease (AD) result from structural and functional deficiencies that generate limitations in the performance of activities and restrictions in individual’s biopsychosocial participation. In a translational way, we have used the conceptual framework proposed by the International Classification of Disability and Health Functioning (ICF) to classify and describe the functioning and disability on gait and exploratory activity in the 3xTg-AD animal model. We developed a behavioral observation method that allows us to differentiate qualitative parameters of psychomoto

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Delgado-Peraza, Francheska, Carlos J. Nogueras-Ortiz, Olga Volpert, et al. "Neuronal and Astrocytic Extracellular Vesicle Biomarkers in Blood Reflect Brain Pathology in Mouse Models of Alzheimer’s Disease." Cells 10, no. 5 (2021): 993. http://dx.doi.org/10.3390/cells10050993.

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Circulating neuronal extracellular vesicles (NEVs) of Alzheimer’s disease (AD) patients show high Tau and β-amyloid (Aβ) levels, whereas their astrocytic EVs (AEVs) contain high complement levels. To validate EV proteins as AD biomarkers, we immunocaptured NEVs and AEVs from plasma collected from fifteen wild type (WT), four 2xTg-AD, nine 5xFAD, and fifteen 3xTg-AD mice and assessed biomarker relationships with brain tissue levels. NEVs from 3xTg-AD mice had higher total Tau (p = 0.03) and p181-Tau (p = 0.0004) compared to WT mice. There were moderately strong correlations between biomarkers i

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González de San Román, Estibaliz, Alberto Llorente-Ovejero, Jonatan Martínez-Gardeazabal, et al. "Modulation of Neurolipid Signaling and Specific Lipid Species in the Triple Transgenic Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 22, no. 22 (2021): 12256. http://dx.doi.org/10.3390/ijms222212256.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia in aging populations. Recently, the regulation of neurolipid-mediated signaling and cerebral lipid species was shown in AD patients. The triple transgenic mouse model (3xTg-AD), harboring βAPPSwe, PS1M146V, and tauP301L transgenes, mimics many critical aspects of AD neuropathology and progressively develops neuropathological markers. Thus, in the present study, 3xTg-AD mice have been used to test the involvement of the neurolipid-based signaling by endocannabinoids (eCB), lysophosphatidic

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Espino de la Fuente-Muñoz, César, Mónica Rosas-Lemus, Perla Moreno-Castilla, Federico Bermúdez-Rattoni, Salvador Uribe-Carvajal, and Clorinda Arias. "Age-Dependent Decline in Synaptic Mitochondrial Function Is Exacerbated in Vulnerable Brain Regions of Female 3xTg-AD Mice." International Journal of Molecular Sciences 21, no. 22 (2020): 8727. http://dx.doi.org/10.3390/ijms21228727.

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Synaptic aging has been associated with neuronal circuit dysfunction and cognitive decline. Reduced mitochondrial function may be an early event that compromises synaptic integrity and neurotransmission in vulnerable brain regions during physiological and pathological aging. Thus, we aimed to measure mitochondrial function in synapses from three brain regions at two different ages in the 3xTg-AD mouse model and in wild mice. We found that aging is the main factor associated with the decline in synaptic mitochondrial function, particularly in synapses isolated from the cerebellum. Accumulation

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Snow, Wanda M., Chris Cadonic, Claudia Cortes-Perez, et al. "Sex-Specific Effects of Chronic Creatine Supplementation on Hippocampal-Mediated Spatial Cognition in the 3xTg Mouse Model of Alzheimer’s Disease." Nutrients 12, no. 11 (2020): 3589. http://dx.doi.org/10.3390/nu12113589.

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The creatine (Cr) energy system has been implicated in Alzheimer’s disease (AD), including reductions in brain phosphoCr and Cr kinase, yet no studies have examined the neurobehavioral effects of Cr supplementation in AD, including the 3xTg mouse model. This studied investigated the effects of Cr supplementation on spatial cognition, plasticity- and disease-related protein levels, and mitochondrial function in the 3xTg hippocampus. Here, 3xTg mice were fed a control or Cr-supplemented (3% Cr (w/w)) diet for 8–9 weeks and tested in the Morris water maze. Mitochondrial oxygen consumption (Seahor

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Kim, Tae-Woon, Sang-Seo Park, Joon-Young Park, and Hye-Sang Park. "Infusion of Plasma from Exercised Mice Ameliorates Cognitive Dysfunction by Increasing Hippocampal Neuroplasticity and Mitochondrial Functions in 3xTg-AD Mice." International Journal of Molecular Sciences 21, no. 9 (2020): 3291. http://dx.doi.org/10.3390/ijms21093291.

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Alzheimer’s disease is the most common neurodegenerative brain disease causing dementia. It is characterized by slow onset and gradual worsening of memory and other cognitive functions. Recently, parabiosis and infusion of plasma from young mice have been proposed to have positive effects in aging and Alzheimer’s disease. Therefore, this study examined whether infusion of plasma from exercised mice improved cognitive functions related to the hippocampus in a 3xTg-Alzheimer’s disease (AD) model. We collected plasma from young mice that had exercised for 3 months and injected 100 µL of plasma in

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Bae, Hyunsu, Hyunjung Baek, Minsook Ye та ін. "Aβ vaccination in conjunction with bee venom derived phospholipase A2 (bvPLA2) ameliorates Alzheimer’s disease pathology through the induction of Aβ-specific Treg population in 3xTg-AD mice". Journal of Immunology 196, № 1_Supplement (2016): 75.18. http://dx.doi.org/10.4049/jimmunol.196.supp.75.18.

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Abstract Alzheimer’s disease (AD) is the most common form of dementia and characterized by an imbalance between the production and clearance of amyloid-beta (Aβ) and tau proteins. Vaccination against Aβ peptide results in dramatic reduction of Aβ pathology in experimental mouse models. Our recent study demonstrated that bvPLA2, the major component of BV, causes immune tolerance by increasing the population of CD4+CD25+Foxp3+ Tregs in cisplatin-induced nephrotoxicity, an allergic asthma and Parkinson disease murine model. Here, we investigated that the effect of bvPLA2 to induce antigen-specifi

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Guzzardi, Maria Angela, Federica La Rosa, Daniela Campani, et al. "Liver and White/Brown Fat Dystrophy Associates with Gut Microbiota and Metabolomic Alterations in 3xTg Alzheimer’s Disease Mouse Model." Metabolites 12, no. 4 (2022): 278. http://dx.doi.org/10.3390/metabo12040278.

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Metabolic impairments and liver and adipose depots alterations were reported in subjects with Alzheimer’s disease (AD), highlighting the role of the liver–adipose–tissue–brain axis in AD pathophysiology. The gut microbiota might play a modulating role. We investigated the alterations to the liver and white/brown adipose tissues (W/BAT) and their relationships with serum and gut metabolites and gut bacteria in a 3xTg mouse model during AD onset (adulthood) and progression (aging) and the impact of high-fat diet (HFD) and intranasal insulin (INI). Glucose metabolism (18FDG-PET), tissue radiodens

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Wei, Wei, Yinghua Liu, Chun-Ling Dai, et al. "Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction." Journal of Alzheimer's Disease 82, no. 2 (2021): 631–46. http://dx.doi.org/10.3233/jad-201599.

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Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance. Cognitive dysfunction and loss of neuronal plasticity are known to begin decades before the clinical diagnosis of the disease. The important influence of congenital genetic mutations on the early development of AD provides a novel opportunity to initiate treatment during early development to prevent the Alzheimer-like behavior and synaptic dysfunction. Objective: To explore strategies for early intervention to prevent Alzheimer’s diseas

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Li, Shuai, Xia Zhao, Philip Lazarovici та Wenhua Zheng. "Artemether Activation of AMPK/GSK3β(ser9)/Nrf2 Signaling Confers Neuroprotection towards β-Amyloid-Induced Neurotoxicity in 3xTg Alzheimer’s Mouse Model". Oxidative Medicine and Cellular Longevity 2019 (21 листопада 2019): 1–24. http://dx.doi.org/10.1155/2019/1862437.

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Alzheimer’s disease is a severe neurodegenerative disease. Multiple factors involving neurofibrillary tangles and amyloid-β plaques lead to the progression of the AD, generated by aggregated hyperphosphorylated Tau protein. Inflammation, mitochondrial dysfunction, and oxidative stress play a significant role in the progression of AD. It has been therefore suggested that the multifactorial nature of AD pathogenesis requires the design of antioxidant drugs with a broad spectrum of neuroprotective activities. For this reason, the use of natural products, characterized by multiple pharmacological

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Martínez-Iglesias, Olaia, Iván Carrera, Juan Carlos Carril, Lucía Fernández-Novoa, Natalia Cacabelos, and Ramón Cacabelos. "DNA Methylation in Neurodegenerative and Cerebrovascular Disorders." International Journal of Molecular Sciences 21, no. 6 (2020): 2220. http://dx.doi.org/10.3390/ijms21062220.

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DNA methylation is an epigenetic mechanism by which methyl groups are added to DNA, playing a crucial role in gene expression regulation. The aim of the present study is to compare methylation status of healthy subjects with that of patients with Alzheimer’s, Parkinson’s or Cerebrovascular diseases. We also analyze methylation status of a transgenic Alzheimer’s disease mouse model (3xTg-AD). Our results show that both global methylation (n = 141) and hydroxymethylation (n = 131) levels are reduced in DNA samples from buffy coats of patients with neurodegenerative disorders and age-related cere

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Torres-Lista, Virginia, and Lydia Giménez-Llort. "Impairment of nesting behaviour in 3xTg-AD mice." Behavioural Brain Research 247 (June 2013): 153–57. http://dx.doi.org/10.1016/j.bbr.2013.03.021.

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Kokras, N., M. Dimitriadou, I. Sotiropoulos, A. L. Skaltsounis, A. Tsarbopoulos, and C. Dalla. "The therapeutic potential of natural compounds against Alzheimer's disease: A preclinical pharmacological study in both sexes." European Psychiatry 33, S1 (2016): S544. http://dx.doi.org/10.1016/j.eurpsy.2016.01.2010.

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Alzheimer's disease (AD), a neurodegenerative neuropsychiatric disorder, is often comorbid with depression and anxiety. Neuropsychiatric disorders are also characterized by sex differences. However, most preclinical pharmacological studies are conducted using only males. Herein, we used male and female twelve-month-old mice (3xTg) expressing mutated forms of human proteins Tau, APP and Presenilin1. These mice are considered a valid animal model of AD. We investigated the effects of the natural compound trans-crocin-4 (TC-4), which is derived from Crocus sativus and the olive compound oleuropei

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Giménez-Llort, Lydia, Yoelvis García, Karla Buccieri, et al. "Gender-Specific Neuroimmunoendocrine Response to Treadmill Exercise in 3xTg-AD Mice." International Journal of Alzheimer's Disease 2010 (2010): 1–17. http://dx.doi.org/10.4061/2010/128354.

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The 3xTg-AD mouse develops a progressive Alzheimer's disease- (AD-) like brain pathology that causes cognitive- and neuropsychiatric-like symptoms of dementia. Since its neuroimmunoendocrine axis is likewise impaired, this mouse is also useful for modelling complex age-related neurodegeneration. This study analyzed behavioral, physiological, neurochemical, pathological and immunoendocrine alterations in male and female 3xTg-AD mice and assayed the effects of a short therapy of forced physical exercise at the moderate pathology stage of 6 months of age. Gender effects were observed in most AD-r

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Chen, Chun, Eun Hee Ahn, Seong Su Kang, Xia Liu, Ashfaqul Alam та Keqiang Ye. "Gut dysbiosis contributes to amyloid pathology, associated with C/EBPβ/AEP signaling activation in Alzheimer’s disease mouse model". Science Advances 6, № 31 (2020): eaba0466. http://dx.doi.org/10.1126/sciadv.aba0466.

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The gut-brain axis is bidirectional, and gut microbiota influence brain disorders including Alzheimer’s disease (AD). CCAAT/enhancer binding protein β/asparagine endopeptidase (C/EBPβ/AEP) signaling spatiotemporally mediates AD pathologies in the brain via cleaving both β-amyloid precursor protein and Tau. We show that gut dysbiosis occurs in 5xFAD mice, and is associated with escalation of the C/EBPβ/AEP pathway in the gut with age. Unlike that of aged wild-type mice, the microbiota of aged 3xTg mice accelerate AD pathology in young 3xTg mice, accompanied by active C/EBPβ/AEP signaling in the

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Muñoz-Montero, Alicia, Ricardo de Pascual, Anabel Sáez-Mas, Inés Colmena, and Luis Gandía. "Alterations of the Sympathoadrenal Axis Related to the Development of Alzheimer’s Disease in the 3xTg Mouse Model." Biology 11, no. 4 (2022): 511. http://dx.doi.org/10.3390/biology11040511.

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Alzheimer’s disease (AD), the most common form of dementia, is becoming a global health problem and public health priority. In the advanced stages of AD, besides the initial cognitive symptoms, behavioral problems, particularly agitation and aggressiveness, become prevalent in AD patients. These non-cognitive symptoms could be related to a noradrenergic overactivation. In this study, we used chromaffin cells (CCs) isolated from the adrenal gland of 3xTg AD model mice to characterize potential alterations in the autocrine-paracrine modulation of voltage-dependent calcium channels (VDCCs), which

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Oblak, Adrian L., Harriet M. Williams, David Baglietto-Vargas, et al. "P1-130: MODEL-AD: CHARACTERIZATION OF FAMILIAL AD MODELS (5XFAD, APP/PS1, HTAU, 3XTG-AD)." Alzheimer's & Dementia 14, no. 7S_Part_5 (2006): P321. http://dx.doi.org/10.1016/j.jalz.2018.06.133.

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Chen, Yi-An, Cheng-Hsiu Lu, Chien-Chih Ke, et al. "Evaluation of Class IIa Histone Deacetylases Expression and In Vivo Epigenetic Imaging in a Transgenic Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 22, no. 16 (2021): 8633. http://dx.doi.org/10.3390/ijms22168633.

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Epigenetic regulation by histone deacetylase (HDAC) is associated with synaptic plasticity and memory formation, and its aberrant expression has been linked to cognitive disorders, including Alzheimer’s disease (AD). This study aimed to investigate the role of class IIa HDAC expression in AD and monitor it in vivo using a novel radiotracer, 6-(tri-fluoroacetamido)-1-hexanoicanilide ([18F]TFAHA). A human neural cell culture model with familial AD (FAD) mutations was established and used for in vitro assays. Positron emission tomography (PET) imaging with [18F]TFAHA was performed in a 3xTg AD mo

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Paula, Pérez-Corredor, Sabogal-Guáqueta Angelica Maria, Carrillo-Hormaza Luis, and Cardona-Gómez Gloria Patricia. "Preventive Effect of Quercetin in a Triple Transgenic Alzheimer’s Disease Mice Model." Molecules 24, no. 12 (2019): 2287. http://dx.doi.org/10.3390/molecules24122287.

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Alzheimer’s disease (AD) is the most common type of dementia and is the leading cause of disability in elderly people worldwide. Current pharmacological therapies do not cure the disease, and for this reason, some pharmacotherapy studies have investigated preventive treatments focused on modifiable nutritional factors such as diet. Quercetin (Qc) is a flavonoid found in fruits and vegetables that has several biological properties. In this study, we evaluated the effect of chronic oral quercetin administration (100 mg/kg) on neurodegeneration markers and cognitive and emotional deficits in a tr

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Ochi, Shinichiro, Jun-ichi Iga, Yu Funahashi, et al. "Identifying Blood Transcriptome Biomarkers of Alzheimer’s Disease Using Transgenic Mice." Molecular Neurobiology 57, no. 12 (2020): 4941–51. http://dx.doi.org/10.1007/s12035-020-02058-2.

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Abstract The testing of pathological biomarkers of Alzheimer’s disease (AD), such as amyloid beta and tau, is time-consuming, expensive, and invasive. Here, we used 3xTg-AD mice to identify and validate putative novel blood transcriptome biomarkers of AD that can potentially be identified in the blood of patients. mRNA was extracted from the blood and hippocampus of 3xTg-AD and control mice at different ages and used for microarray analysis. Network and functional analyses revealed that the differentially expressed genes between AD and control mice modulated the immune and neuroinflammation sy

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Bello-Medina, Paola C., Karina Corona-Cervantes, Norma Gabriela Zavala Torres та ін. "Chronic-Antibiotics Induced Gut Microbiota Dysbiosis Rescues Memory Impairment and Reduces β-Amyloid Aggregation in a Preclinical Alzheimer’s Disease Model". International Journal of Molecular Sciences 23, № 15 (2022): 8209. http://dx.doi.org/10.3390/ijms23158209.

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Alzheimer’s disease (AD) is a multifactorial pathology characterized by β-amyloid (Aβ) deposits, Tau hyperphosphorylation, neuroinflammatory response, and cognitive deficit. Changes in the bacterial gut microbiota (BGM) have been reported as a possible etiological factor of AD. We assessed in offspring (F1) 3xTg, the effect of BGM dysbiosisdysbiosis in mothers (F0) at gestation and F1 from lactation up to the age of 5 months on Aβ and Tau levels in the hippocampus, as well as on spatial memory at the early symptomatic stage of AD. We found that BGM dysbiosisdysbiosis with antibiotics (Abx) tre

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