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Dissertations / Theses on the topic '3xtg-AD'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Kinoshita, Denise. "Análise temporal de mediadores inflamatórios no tecido neuronal e na periferia em camundongos 3xTg-AD, um modelo animal para a Doença de Alzheimer." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-26092012-140403/.

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A Doença de Alzheimer é a causa mais freqüente de demência senil e os gastos com pacientes com demência já supera os de pacientes com câncer ou com doenças cardiovasculares. As lesões características dessa doença são as placas amilóides e os emaranhados neurofibrilares. A neuroinflamação também está presente na maioria dos pacientes com Alzheimer, e parece contribuir para o dano no tecido neuronal. Adicionalmente, estudos vêm demonstrando que pacientes com Alzheimer também apresentam alterações sistêmicas, e, dessas, a mais relatada é o estado pró-inflamatório em tecidos periféricos, permitind

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12

Torres-Lista, Virginia. "Conducta social, anidación y respuesta a antipsicóticos Atípicos en el modelo triple transgénico 3xtg-AD para la Enfermedad de alzheimer." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/117537.

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A pesar de que la demencia es el síntoma característico de la enfermedad de Alzheimer, los síntomas conductuales y psicológicos asociados a ella (SCPD) y las alteraciones en las actividades de la vida diaria (AVD) son problemas comunes en los pacientes que sufren la enfermedad. SCPD y AVD causan angustia y discapacidad de forma considerable en los enfermos, generan síndromes relacionados con estrés en sus cuidadores y son considerados los principales causantes de la institucionalización temprana de los pacientes. Modelar a nivel experimental este amplio espectro de síntomas es difícil, pero

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13

Esquerda, Canals Gisela. "New insights into alzheimer’s disease: further characterization of the 3xTg-AD mouse model and a pharmacological approach with scFv-h3D6." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/462035.

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La malaltia d’Alzheimer és el desordre neurodegeneratiu més comú arreu del món. L’acumulació del pèptid beta-amiloide (Aβ) és el principal factor en el seu patomecanisme. El model murí 3xTg-AD ha esdevingut un dels models més populars d’aquesta malaltia perquè manifesta la patologia Aβ i tau seguint un patró regional i temporal similar als humans. Per una banda, aquesta tesi consisteix en la caracterització del model 3xTg-AD a 5 mesos d’edat, mitjançant tècniques bioquímiques, histològiques i conductuals. S’ha observat que, en aquesta edat, les neurones glutamatèrgiques són les que es troben

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14

Kil, Eric Joon Bum. "CRISPR-Cas9 mediated HMGCL KO in 3xTg AD mice reduces the cognitive deficit improvement seen in an intermittent metabolic switching regimen." Scholarship @ Claremont, 2018. http://scholarship.claremont.edu/cmc_theses/1832.

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Individuals in modern Western societies are experiencing increasing sedentary lifestyles, overindulgence of high fat, high-sugar diets, and extremely sterilized conditions, putting immense pressure on researchers and clinicians alike to come up with viable treatments for conditions implicated with an aging society. Emerging research have published the benefits of IMS and metabolic switching in a variety of neuroprotective, cellular stress resistance, and neuroplasticity pathways in animal models and clinical results from randomized trials of IMS regimens with susceptible human populations are

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15

Oliveira, Catarina Luísa da Silva Lopes e. Campos de. "Identificação e quantificação de gangliósidos em cérebro de modelos animais de doença de Alzheimer: um estudo lipidómico." Master's thesis, Universidade de Aveiro, 2016. http://hdl.handle.net/10773/17731.

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Mestrado em Bioquímica, ramo de Métodos Biomoleculares<br>A doença de Alzheimer é uma doença neurodegenerativa, sendo a forma mais comum de demência. As projeções para 2030 apontam para 75,6 milhões de casos, e o triplo para 2050. A doença de Alzheimer é caracterizada pela presença de deposição do péptido β-amilóide e tranças neurofibrilares. Durante o processo neurodegenerativo, as propriedades físico-químicas das membranas são alteradas. Esta alteração pode resultar de uma desregulação nas proporções dos fosfolípidos e gangliósidos e/ou de mudanças nos rácios. Assim, o objetivo principal des

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16

Güell, Bosch Jofre. "Diagnòstic i monitorització de la malaltia d’Alzheimer mitjançant tècniques de ressonància magnètica in vivo en el model 3xTg-AD: Avaluació de l’eficàcia del tractament longitudinal amb dos fragments d’anticòs contra el pèptid Aβ". Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457363.

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La malaltia d’Alzheimer (AD) és, actualment, una malaltia incurable que afecta la major part dels 47 milions de persones que s’estima que pateixen demència arreu del món. Tot i que els mecanismes que donen lloc a desenvolupar l’AD no estan ben definits, hi ha un consens bastant ampli en acceptar la hipòtesi de la cascada amiloide, la qual situa el pèptid Aβ o, més concretament, els oligòmers que forma aquest pèptid, com els responsables principals de l’inici del procés neuropatològic que porta a l’AD. En els últims anys la immunoteràpia anti-Aβ s’ha erigit com una eina esperançadora per trac

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17

Rivera, Hernández Geovanny. "Obtención de un fragmento de anticuerpo específico contra oligómeros de Aβ como agente inmunoterapéutico de la enfermedad de Alzheimer: demostración de su eficacia en el modelo murino 3xTg-AD y mejora de su estabilidad termodinámica". Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/133326.

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La enfermedad de Alzheimer (AD) se ha convertido en un problema de primer orden en países desarrollados debido al coste sanitario social y humano que conlleva. La hipótesis de la cascada amiloide, la más aceptada por la comunidad científica, sitúa al péptido Aβ como el responsable directo del proceso neuropatológico, concretamente a los oligómeros de Aβ. En la actualidad, existen multiples tratamientos sintomáticos-paliativos, sin que ningúno se haya descrito como curativo. Recientemente, la inmunoterapia β-amiloide se ha revelado como una posible herramienta en el tratamiento de la AD. En co

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18

Pais, Vera Cristina Martinho. "Effect of class I histone deacetylase inhibitors in 3xTg-AD mice." Master's thesis, 2019. http://hdl.handle.net/10773/26899.

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Alzheimer’s disease is the commonest form of dementia worldwide. Clinically, this neurodegenerative disorder is characterized by cognitive decline, changes in personality and mood, and disorientation. Neuropathologically, it is characterized by the extracellular accumulation of beta-amyloid peptide (Aβ) forming senile plaques, and the intracellular deposition of hyperphosphorylated Tau protein forming neurofibrillary tangles. Alzheimer’s disease affects primarily the hippocampus and may progress towards the cerebral cortex. Recent studies showed that deregulation of histone acetylation is asso

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19

Carecho, Rafael José Monteiro. "Can the retina be a window to the changing brain in Alzheimer's disease?" Master's thesis, 2017. http://hdl.handle.net/10316/81429.

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Dissertação de Mestrado em Investigação Biomédica apresentada à Faculdade de Medicina<br>Alzheimer’s disease (AD) became the most common neurodegenerative disorder worldwide, as a consequence of a growing elderly population. AD is a multifactorial disorder characterized by the accumulation of amyloid-beta (Aβ) plaques followed by neurofibrillary tangles of hyperphosphorylated tau protein leading to a massive neuronal loss and brain homeostasis disruption. These alterations result in severe cognitive impairments and memory loss having a huge impact in AD patient’s life. So far, AD does not have

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20

Hsu, Hung-Cheng, and 許弘政. "Treatment of late-stage Alzheimer's disease with folate derivatives in the 3xTg-AD mice model." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/78636392051847292027.

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碩士<br>輔仁大學<br>營養科學系碩士班<br>101<br>Cell line and animal model had indicated that folate supplementation could help lower homocysteine levels and decrease oxidative stress. We have previously reported that folic acid potentiated effects of Alzheimer’s disease (AD) drug on neuronal protection in early-stage AD development. Folic acid is a kind of nutrient supplement, and folinic acid is a clinical cancer drug. However, in this study, the treatment of late-stage AD with folate derivatives in 3xTg-AD transgenic mice was investigated. Forty 3xTg-AD mice at 16 month-old were divided into three groups

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21

Stover, Kurt. "Effects of Maternal Environment on Behavioural Development in Young Adult 3xTg-AD and B6129S/F2 Mice." 2012. http://hdl.handle.net/10222/15149.

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The 3xTg-AD mouse model of Alzheimer’s disease (AD) has three transgenes, one human gene from familial AD (APPswe), one mutated mouse gene (PS1M1461), and one human gene associated with tau pathology (tauP301L). Transgenic and wildtype (B6129S/F2) mice must be bred as separate lines. We cross fostered litters of transgenic and wildtype mice and measured their behaviour at two and six months of age. We found that transgenic mice had lowered anxiety-like behaviours, decreased locomotion, and improved motor performance at two and six months of age. Transgenic mice had a deficit in visuo-spatial l

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22

Fu, Chen-Huan, and 傅晨歡. "Effects of oropharyngeal aspiration to diesel exhaust particles on central nervous system toxicity in 3xTg-AD mice." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/nq59ns.

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碩士<br>國立臺灣大學<br>職業醫學與工業衛生研究所<br>107<br>Air pollution has been known as a major health threat for decades. Many epidemiological and toxicological studies of air pollution have confirmed that ambient particulate matter can cause adverse effects on the central nervous system (CNS), including neuroinflammation, oxidative stress, autophagy dysfunction and contribute to neurodegenerative diseases, such as Alzheimer’s disease (AD). In the modern city, the most important source of pollution is traffic-related air pollutants. Diesel exhaust particles (DEPs) emitted by diesel engine combustion is the mo

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23

Fraser, Leanne M. "Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study." Thesis, 2013. http://hdl.handle.net/10222/28080.

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The triple transgenic (3xTg-AD) mouse model of Alzheimer’s disease (AD) possesses three transgenes that lead to the development of amyloid-beta (A?) plaques (APPswe, PS1M146V) and neurofibrillary tangles (and tauP301L) (Oddo et al., 2003b). Although the neuropathology of these mice has been extensively studied (Sy et al., 2011), less research has been done to investigate their working memory, emotionality, and locomotor-related behaviour. Using a cross-sectional design, male and female 3xTg-AD mice were compared to control mice (B6129SF2/J) at five ages (2-, 6-, 9-, 12-, and 15-months of age)

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Chuang, Ching, and 莊晴. "Ambient particles exposure and progress of Alzheimer''s disease in 3xTg-AD mice: a pilot study." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/84t7ev.

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碩士<br>國立臺灣大學<br>職業醫學與工業衛生研究所<br>105<br>Many studies have shown that particulate matter (PM) may have adverse effects on the human body. PM has been associated with mortality and morbidity of cardiopulmonary diseases. PM may affect the CNS by two pathways, through the direct or peripheral way. In the peripheral way, systemic inflammation induced by PM and transfer inflammatory response to the brain by enhanced neuroinflammation and oxidative stress. PM might contribute to neurodegeneration diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease. Alzheimer’s disease is a progressive n

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25

Yagensky, Oleksandr. "Identifying stage-specific markers of Alzheimer's disease using quantitative proteomics." Doctoral thesis, 2018. http://hdl.handle.net/11858/00-1735-0000-002E-E4A6-D.

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Chou, Chien-Yu, and 周千祐. "Effects of Folate Intakes in Regulation of Alzheimer’s Disease Associated Pathological, Mitochondrial Abnormalities and Cognitive Function in Aged C57BL/6 Mice and 3xTg-AD Mice." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/05955930250982121474.

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碩士<br>輔仁大學<br>營養科學系碩士班<br>103<br>Alzheimer’s disease (AD) is the most common degenerative dementia. β-amyloid protein (Aβ), neurofibrillary tangles (NFTs, consisted of tau protein) deposit and mitochondrial dysfunction in hippocampus and cortex is the pathology of Alzheimer’s disease (AD). It has been known that folate supplementation can improve mitochondrial function and it can decrease AD risk factor. However, most patients were detected that they suffered from AD until late-stage of AD. Whether folate supplementation in this stage can improve mitochondrial shape and function then further d

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