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Artykuły w czasopismach na temat "3xtg-AD"

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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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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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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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Rozprawy doktorskie na temat "3xtg-AD"

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Ioshimoto, Gabriela Lourençon. "Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD)." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/.

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Objetivo: Avaliar eletrofisiologicamente a função da retina do camundongo modelo de Alzheimer (3xTg-AD) comparando com seu controle (b6;129-PS1) em um estudo longitudinal com seis idades (2, 4, 6, 8, 10 e 12 meses). Métodos: Eletrorretinogramas (ERGs) foram registrados em 44 camundongos 3xTg-AD e em 23 controles, após administrada anestesia. Para o registro foi colocado um eletrodo de lente de contato sobre a córnea, um eletrodo de referência na cabeça e um terra na cauda. Em sessão de 30-40min de duração foram expostos ao seguinte protocolo de estimulação: 1) Adaptação ao escuro seguida de f
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McNicoll, Marie-Michelle. "Early Defects in Neurogenesis in the 3xTg Mouse Model of AD." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42665.

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Branca, Caterina, Darren M. Shaw, Ramona Belfiore, et al. "Dyrk1 inhibition improves Alzheimer's disease-like pathology." WILEY, 2017. http://hdl.handle.net/10150/626504.

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There is an urgent need for the development of new therapeutic strategies for Alzheimer's disease (AD). The dual-specificity tyrosine phosphorylation-regulated kinase-1A (Dyrk1a) is a protein kinase that phosphorylates the amyloid precursor protein (APP) and tau and thus represents a link between two key proteins involved in AD pathogenesis. Furthermore, Dyrk1a is upregulated in postmortem human brains, and high levels of Dyrk1a are associated with mental retardation. Here, we sought to determine the effects of Dyrk1 inhibition on AD-like pathology developed by 3xTg-AD mice, a widely used anim
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Baeta, Corral Raquel. "Factors de risc en la malaltia d’Alzheimer: Estudis en animals triple transgènics 3xTg-AD." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285546.

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El principal factor de risc en la malaltia d’Alzheimer, la demència senil més freqüent, és l’edat i presenta major incidència en les dones. En la seva aparició, se li atribueixen també altres factors de risc, tant biològics (genètics i no genètics) com ambientals. La seva forma familiar heretada genèticament (< 5% dels casos), i l’esporàdica (majoritària, d’etiologia desconeguda) difereixen en l’edat d’inici i la taxa de progressió del procés neurodegeneratiu. Tot i això, el fet que comparteixin els mateixos símptomes cognitius i els conductuals i psicològics associats a la demència (BPSD) aix
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PACE, LORENZO. "Behavioral and neurochemical effects of Palmitoylethanolamide in a murine model of Alzheimer’s Disease." Doctoral thesis, Università di Foggia, 2016. http://hdl.handle.net/11369/338930.

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Abstract La malattia di Alzheimer è la forma più comune di demenza degenerativa progressivamente invalidante con esordio prevalentemente in età presenile. Si stima che circa il 60-70% dei casi di demenza sia dovuta a Alzheimer disease (AD). AD è una patologia multifattoriale caratterizzata sia da placche senili extracellulari, costituite dall’accumulo della proteina amiloide, sia da grovigli neurofibrillari intracellulari, composti da filamenti Tau patologici (NFTs). Inoltre nell’Alzheimer vi è anche perdita neuronale soprattutto a livello delle aree cerebrali che sottendono i processi di a
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Vandal, Milène. "Interrelation entre déficits métaboliques et neuropathologie associée à la maladie d'Alzheimer chez la souris 3xTg-AD." Doctoral thesis, Université Laval, 2016. http://hdl.handle.net/20.500.11794/26779.

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Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2015-2016<br>La maladie d’Alzheimer (MA) est la maladie neurodégénérative qui cause le plus important nombre de cas de démence. On estime que près de 15% des canadiens âgés de plus de 65 ans sont atteints de la MA. Avec le vieillissement de la population, le nombre de cas augmentera de manière substantielle dans les prochaines années. À l’heure actuelle, aucun traitement ne permet de ralentir la progression de la maladie. Pour plus de 99% des cas, ses causes exactes demeurent indéterminées. Toutefois, de nombreux facteur
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Jones, Torrie Turner. "Age-Related Deficits in Electron Transport Chain Complexes in Rat Neurons and 3xTg-AD Mouse Neurons." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1797219571&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (Ph. D.)--Southern Illinois University Carbondale, 2009.<br>"Department of Molecular Biology, Microbiology, and Biochemistry." Keywords: Aging, Cytochrome c oxidase, Electron transport chains, Estrogen, Mitochondria, Neurons. Includes bibliographical references (p. 102-137). Also available online.
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García, Mesa Yoelvis. "El ejercicio físico voluntario como terapia para la enfermedad de Alzheimer: Estudio en ratones tripletransgénicos 3xTg-AD." Doctoral thesis, Universitat de Barcelona, 2010. http://hdl.handle.net/10803/2334.

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La enfermedad de Alzheimer (EA) es una patología neurodegenerativa, progresiva y compleja que fue descrita por primera vez hace más de 100 años. Está considerada dentro del grupo de las demencias, siendo de estas la más frecuente (López-Pousa et al., 1999). Clínicamente la enfermedad se presenta con la pérdida progresiva de la memoria de corto alcance y a medida que avanza se produce la pérdida de la memoria de larga duración y el pensamiento abstracto. En la etapa más tardía de la enfermedad los pacientes se vuelven confusos y pierden la orientación del lugar y del tiempo. Estas manifestacion
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Castaño, Prat Patricia. "Oscilaciones lentas en la red cortical alterada: una caracterización de los modelos murinos 3xTg-AD, SAMP8 y Fmr1KO." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/593487.

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A lo largo de esta tesis se han utilizado las oscilaciones lentas (SO), que emergen durante el sueño de onda lenta y bajo el efecto de ciertos tipos de anestesia, como paradigma para detectar alteraciones funcionales en la corteza de varios modelos murinos de la Enfermedad de Alzheimer (AD) y el Síndrome X Frágil (FXS), para monitorizar la progresión de su enfermedad, y para evaluar la efectividad de dos intervenciones terapéuticas. La caracterización detallada de los parámetros de las SO en varias áreas corticales de los modelos de la AD 3xTg-AD y SAMP8 mostró que dichos parámetros se alter
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Escrig, Monfort Anna. "Interleukin-6 trans-signaling in Alzheimer's disease. A study based on the Tg2576 and 3xTg-AD mouse models." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667955.

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Części książek na temat "3xtg-AD"

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Sy, Michael, Masashi Kitazawa, and Frank LaFerla. "The 3xTg-AD Mouse Model: Reproducing and Modulating Plaque and Tangle Pathology." In Neuromethods. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-898-0_24.

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Ferreira, Hugo, João Martins, Ana Nunes, et al. "Characterization of the Retinal Changes of the 3xTg-AD Mouse Model of Alzheimer’s Disease." In IFMBE Proceedings. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-31635-8_220.

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Chabrier, Meredith A., Kara M. Neely, Nicholas A. Castello, and Frank M. LaFerla. "The Contribution of Transgenic Models to the Understanding of Alzheimer's Disease Progression and Therapeutic Development." In Animal Models for Neurodegenerative Disease. The Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/bk9781849731843-00001.

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Transgenic mouse models of Alzheimer disease (AD) have been invaluable in unraveling the mechanisms of disease progression and for testing potential therapeutic interventions. Since the cause of sporadic AD is unknown, transgenic models of AD are primarily based on mutations found only in patients with familial AD. These mutations produce pathological and cognitive changes that resemble sporadic AD, and thus these transgenic mice are still extremely useful for studying this more common form of AD. Here we discuss notable advances in our understanding of AD pathogenesis that have directly resulted from studies with transgenic models of AD, such as the finding from 3xTg-AD mice and other models demonstrating that tau pathology is facilitated by amyloid-beta. We also discuss several promising therapeutics that were largely characterized using transgenic mice, including immunotherapy, HDAC inhibitors, and M1 receptor agonists.
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Syeda, Tauqeerunnisa, Mónica Sanchez-Tapia, Laura Pinedo-Vargas, et al. "Bioactive Food Abates Metabolic and Synaptic Alterations by Modulation of Gut Microbiota in a Mouse Model of Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220018.

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Recent investigations have demonstrated an important role of gut microbiota (GM) in the pathogenesis of Alzheimer’s disease (AD). GM modulates a host’s health and disease by production of several substances, including lipopolysaccharides (LPS) and short-chain fatty acids (SCFAs), among others. Diet can modify the composition and diversity of GM, and ingestion of a healthy diet has been suggested to lower the risk to develop AD. We have previously shown that bioactive food (BF) ingestion can abate neuroinflammation and oxidative stress and improve cognition in obese rats, effects associated with GM composition. Therefore, BF can impact the gut-brain axis and improved behavior. In this study, we aim to explore if inclusion of BF in the diet may impact central pathological markers of AD by modulation of the GM. Triple transgenic 3xTg-AD (TG) female mice were fed a combination of dried nopal, soy, chia oil, and turmeric for 7 months. We found that BF ingestion improved cognition and reduced Aβ aggregates and tau hyperphosphorylation. In addition, BF decreased MDA levels, astrocyte and microglial activation, PSD-95, synaptophysin, GluR1 and ARC protein levels in TG mice. Furthermore, TG mice fed BF showed increased levels of pGSK-3β. GM analysis revealed that pro-inflammatory bacteria were more abundant in TG mice compared to wild-type, while BF ingestion was able to restore the GM’s composition, LPS, and propionate levels to control values. Therefore, the neuroprotective effects of BF may be mediated, in part, by modulation of GM and the release of neurotoxic substances that alter brain function.
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Hoffman, Jessica L., Sara Faccidomo, Michelle Kim, et al. "Alcohol drinking exacerbates neural and behavioral pathology in the 3xTg-AD mouse model of Alzheimer's disease." In International Review of Neurobiology. Elsevier, 2019. http://dx.doi.org/10.1016/bs.irn.2019.10.017.

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Streszczenia konferencji na temat "3xtg-AD"

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Alveal-Mellado, Daniel, and Lydia Giménez-Llort. "Sex-Dependent Variations in Voluntary Exercise of 14-Month-Old 3xTg-AD Mice Associated with Novelty Inhibition." In IECBS 2022. MDPI, 2022. http://dx.doi.org/10.3390/iecbs2022-12946.

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Fraile-Ramos, Juan, and Lydia Giménez-Llort. "Sex-Dependent Hepatomegaly, and Increased Hepatic Oxidative Stress in Old Male and Female 3xTg-AD Mice as Compared to Mice with Physiological Aging." In IECBS 2021. MDPI, 2021. http://dx.doi.org/10.3390/iecbs2021-10668.

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Pérez-Gozalbo, Clara, and Lydia Giménez-Llort. "Obesity, Impaired Glucose Metabolism and Hepatic Histopathological Damage in 3xTg-AD Mice at Different Stages of Disease Compared to Mice with Normal Aging." In IECBS 2022. MDPI, 2022. http://dx.doi.org/10.3390/iecbs2022-12938.

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