Dissertations / Theses on the topic 'Epigenetic memory'
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Magnell, Albert T. (Albert Thomas). "Epigenetic Memory of Mouse Intestinal Inflammation." Thesis, Massachusetts Institute of Technology, 2021. https://hdl.handle.net/1721.1/130670.
Full textCataloged from the official PDF version of thesis.
Includes bibliographical references (pages 29-31).
The gut, encompassing one of the largest epithelial surfaces in the body, interacts with both biological and non-biological agents that can cause regular injury. Fortunately, the small intestinal epithelium has a remarkable capacity to repair itself after severe injury, due to the abundance of highly replicative stem cells housed in the intestinal crypt regions. Much remains to be understood about the activation processes of the repair mechanisms and to what extent the stem cells themselves can adapt to certain forms of damage, including molecular mechanisms related to gene regulation. Here, I show that in response to acute inflammation, chromatin in intestinal stem cells has increased accessibility around specific loci and that this state is maintained in some regions even after the epithelium has recovered from damage, suggesting the possibility of memory. Such epigenetic memory may confer some adaptive resiliency to subsequent damage.
by Albert T. Magnell.
S.M.
S.M. Massachusetts Institute of Technology, Department of Biology
Chandramohan, Yalini. "Epigenetic mechanisms underlying stress-related learning and memory." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492580.
Full textGookin, Dylon Kyle. "Epigenetic Mechanisms for Long-Term Memory Acquisition and Maintenance." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579049.
Full textCherubini, A. "MYC-DRIVEN EPIGENETIC MEMORY MAINTAINS EMBRYONIC STEM CELL IDENTITY." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/356044.
Full textKłosin, Adam 1985. "Mechanism and dynamics of transgenerational epigenetic memory in Caenorhabditis elegans." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/482206.
Full textSince Darwin and Lamarck, biologists have been intrigued by the possibility of the inheritance of environmentally-acquired traits. Examples of inter-generational transmission of traits induced by an environmental perturbation have been reported in multiple species, but the molecular mechanisms governing these responses remain obscure. Using C. elegans as a model system we demonstrate that high temperature-induced increase in expression from a somatically expressed transgene array persists for multiple generations. This epigenetic memory is governed by transgenerational transmission of two conflicting epigenetic memories: H3K9me3 histone marks are inherited in cis and act as the major determinant of expression levels in the next generation, whereas repressive small RNAs are inherited in trans and mediate restoration of the repressed state. In addition, epigenetic resetting is reinforced by soma to germline communication mediated by the dsRNA channel SID-1. Finally, we discovered that replication stress during early embryonic development interferes with epigenetic inheritance of a repressed state. These findings contribute to our understanding of the epigenetic inheritance and eventual resetting of environmentally acquired traits.
Boudadi, Elsa. "Histone modification, gene regulation and epigenetic memory in embryonic stem cells." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3160/.
Full textNg, Kit. "Epigenetic memory of donor cell differentiation status in Xenopus nuclear transplant embryos." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615284.
Full textVIGORELLI, VERA. "CD34+ stem cells and epigenetic memory: key players and pharmacological targets in diabetic cardiovascular complication." Doctoral thesis, Università degli studi di Pavia, 2020. http://hdl.handle.net/11571/1371994.
Full textSeaborne, R. A. "The role of DNA methylation in the regulation of skeletal muscle atrophy, hypertrophy and epigenetic 'memory'." Thesis, Liverpool John Moores University, 2018. http://researchonline.ljmu.ac.uk/9473/.
Full textWendeln, Ann-Christin [Verfasser]. "Long-lasting epigenetic microglial memory of peripheral inflammation modulates hallmarks of Alzheimer's disease pathology / Ann-Christin Wendeln." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1217249214/34.
Full textLONGARETTI, ALESSANDRA. "EPIGENETIC HOMEOSTATIC MECHANISM IN NEURONAL ADAPTATION AND METAPLASTICITY TO ENVIRONMENTAL STIMULI." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/796757.
Full textConine, Colin C. "Small RNAs and Argonautes Provide a Paternal Epigenetic Memory of Germline Gene Expression to Promote Thermotolerant Male Fertility: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/724.
Full textConine, Colin C. "Small RNAs and Argonautes Provide a Paternal Epigenetic Memory of Germline Gene Expression to Promote Thermotolerant Male Fertility: A Dissertation." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/724.
Full textCitir, Gozde. "A Study On Cobalt Adaptation And Memory Retention Of Freshwater Bacteria Isolates." Master's thesis, METU, 2010. http://etd.lib.metu.edu.tr/upload/12612824/index.pdf.
Full textLesburgueres, Edith. "Implication fonctionnelle de l’interface hippocampo-corticale dans le processus de consolidation systémique de la mémoire associative non spatiale chez le rat : contribution du mécanisme d’étiquetage neuronal." Thesis, Bordeaux 1, 2009. http://www.theses.fr/2009BOR13982/document.
Full textAbstract :
Carrasco, Wong Ivo [Verfasser], and Paola [Akademischer Betreuer] Casanello. "Oxidative stress-induced epigenetic transcriptional memory as a mechanism of programmed endothelial dysfunction in large for gestational age newborn of women with obesity / Ivo Carrasco Wong ; Betreuer: Paola Casanello." Regensburg : Universitätsbibliothek Regensburg, 2019. http://d-nb.info/118990537X/34.
Full textLizotte, Farah. "Mémoire hyperglycémique dans la néphropathie diabétique : implication potentielle de SHP-1." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6980.
Full textAbstract : Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Renal podocytes apoptosis induced by hyperglycemia is an early event of DN. Clinical studies have shown that intensive blood glucose control reduced the development of DN but is not sufficient, if started late, to prevent its progression, introducing the concept of “hyperglycemic memory”. We have recently published that the tyrosine phosphatase SHP-1 is elevated in renal cortex of type 1 diabetic mice (Akita), contributing to insulin unresponsiveness and DN. We hypothesized that SHP-1 expression remains elevated regardless of systemic blood glucose normalization, and is responsible for hyperglycemic memory in podocytes leading to DN progression. In vivo contribution of SHP-1 in hyperglycemic memory was evaluated using Akita mice treated with insulin implants after 4 months of diabetes. Both urinary albuminuria and glomerular filtration rate were significantly increased in diabetic mice compared to non-diabetic mice and remained elevated despite normalization of blood glucose levels. Renal dysfunction was associated with a persistent increase of SHP-1 expression in renal cortex and inhibition of insulin action that were not normalized following insulin implants. Mouse podocytes were cultured in normal (5.6mM; NG), high glucose concentrations (25mM; HG) for 120 h or HG (96 h) followed by NG for an additional 24 h (HG+NG). We observed that Akt and ERK phosphorylation induced by insulin was inhibited in HG and were not restored despite returning glucose level to 5.6 mM after the HG period. This inhibition was associated with persistent increase of SHP-1 expression and phosphatase activity, leading to insulin signaling pathway inhibition. Moreover, caspase 3/7 activity in podocytes exposed to HG was higher than in podocytes cultured in NG and returning glucose concentrations to normal range for the last 24 h after the 96 h HG exposure had no effect on reducing caspase 3/7 activity. Epigenetic changes were studied to explain the hyperglycemic memory effect. On SHP-1 promoter, H3K4me1 levels, an activation mark, tended to be more elevated in podocytes exposed to HG and were maintained despite returning to NG levels after the HG conditions. In conclusion, hyperglycemia induces persistent and epigenetic changes of SHP-1 causing insulin unresponsiveness in the podocytes contributing to DN progression.
Fontoura, Tamiris Schaeffer. "Avaliação transgeracional dos efeitos da dieta hipercalórica sobre o metabolismo e cognição em ratos." Universidade Federal de Juiz de Fora (UFJF), 2017. https://repositorio.ufjf.br/jspui/handle/ufjf/5665.
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A obesidade é um distúrbio multifatorial complexo causada por fatores genéticos e epigenéticos, dentre outros. Um meio intra-uterino adverso, com excesso ou escassez de alimentos pode expor o feto ao desenvolvimento da síndrome metabólica, diabetes e doenças cardiovasculares quando adultos, podendo ser passado transgeracionalmente através de alterações epigenéticas. O exercício físico é uma forma não medicamentosa de prevenção e tratamento da obesidade, melhorando a aptidão cardiorrespiratória e composição corporal, dentre outros fatores. Este estudo avaliou se a dieta rica em sacarose e lipídios dada a fêmeas da geração F0 durante toda sua vida, incluindo gestação e lactação, afetaria os níveis de ansiedade e os padrões de memória transgeracionalmente e se o exercício físico possui efeito protetor sobre os mesmos parâmetros. Ratas da geração F0 foram distribuídas em quatro grupos: controle sedentário (CSed) e exercitado (CEx); dieta sedentário (DSed) e exercitado (DEx). Dos 21 aos 120 dias de vida os animais realizaram treinamento físico em esteira, com intensidade de moderada a intensa, e os animais controle receberam dieta normocalórica e os animais dieta receberam a dieta high sugar/ high fat (HS/HF) no mesmo período. Machos e fêmeas da geração F1 e F2 foram distribuídos em grupos iguais ao da geração materna ao qual pertenciam; porém, consumiram a ração normocalórica e não realizaram treinamento físico. Foi acompanhado o consumo alimentar dos animais e a evolução do peso corporal dos mesmos. Aos 80 dias, foi realizado teste oral de tolerância à glicose (TOTG). Aos 90 dias, todos os animais foram submetidos a testes, para avaliação do nível de ansiedade (labirinto em cruz elevado) memórias de trabalho (30 seg) e longo prazo (24h) (teste de esquiva inibitória). Aos 110 dias, houve a eutanásia e os parâmetros biométricos foram avaliados. A dieta normocalórica e o treinamento físico realizado pela geração F0 promoveram menor acúmulo de gordura nos filhotes machos e fêmeas da geração F1 quando comparados ao CSed1 (gordura retroperitonial: 37,7% nas fêmeas e 27,6% nos machos; gordura perigonadal: 28,16% nos machos). Diferentemente do que aconteceu na geração F1, os machos do grupo DSed2 apresentaram um maior acúmulo de gordura perigonadal, 19,4%, quando comparados ao grupo Csed2. Adicionalmente, o efeito protetor do treinamento físico com relação ao menor acúmulo de gorduras retroperitoniais e perigonadais na geração F2 só aconteceu no grupo DEx2 e nos machos, com redução de 21% e 26,8%, respectivamente, em relação ao grupo DSed2. As fêmeas dos grupos DSed das gerações F1 e F2 não ficaram intolerantes a glicose, contudo houve redução de 11,2% na glicemia das fêmeas do grupo DEx1 quando comparadas ao grupo DSed1. Ao contrário do que aconteceu nas fêmeas da primeira geração, os machos do grupo DSed1 ficaram intolerantes a glicose, com aumento da glicemia em 18,45% quando comparados ao grupo CSed1. O grupo DEx1 e DEx2 apresentaram redução da glicemia em 18,45% e 24,75% quando comparados ao grupo DSed. A dieta HS/HF consumida pela geração F0 reduziu a memória de longo prazo das fêmeas do grupo DSed2 em 88,6% quando comparadas ao grupo CSed2. Também aumentou os níveis de ansiedade dos animais machos da geração F1 do grupo DSed1 em relação aos grupos CSed1 e DEx1. A dieta HS/HF aumentou o nível de ansiedade dos machos da geração F1 e causou prejuízo na memória de longo prazo das fêmeas da geração F2, além de aumentar a glicemia dos filhotes machos do grupo dieta da primeira geração e, causar maior acúmulo de gordura na geração F2. O treinamento físico teve efeito protetor sobre a glicemia da descendência, reduziu a adiposidade dos filhotes machos e fêmeas de F1 (grupo controle). Tal efeito só se manteve na geração F2 nos filhotes machos do grupo dieta. A dieta HS/HF consumida por fêmeas desde o desmame até a lactação altera o metabolismo, a memória e os níveis de ansiedade nas gerações F1 e F2, particularmente entre os machos. O treinamento físico de intensidade moderada a intensa realizada pela geração F0 protege a progênie.
Obesity is a complex multifactorial disorder caused by genetic and epigenetic factors, among others. An adverse intrauterine environment with excess or scarcity of food may expose the fetus to the development of metabolic syndrome, diabetes, and cardiovascular disease in adults, and may be transgenerationally passed through epigenetic changes. Physical exercise is a non-medicated form of prevention and treatment of obesity, improving cardiorespiratory fitness and body composition, among other factors. This study evaluated whether the diet rich in sucrose and lipids given to females of the F0 generation throughout their life, including gestation and lactation, would affect anxiety levels and memory patterns transgenerationally and if physical exercise has protective effect on the same parameters. Rats of the F0 generation were divided into four groups: sedentary (CSed) and exercised (CEx) controls; Sedentary (DSed) and exercise diet (DEx). From 21 to 120 days of age, the animals performed physical training on a treadmill at moderate to high intensity, and the control animals received normocaloric diet and the diet animals received the high sugar / high fat (HS / HF) diet during the same period. Males and females of the F1 and F2 generation were distributed in equalgroupsl to the maternal generation to which they belonged; however, consumed the normocaloric chow and did not perform physical training. The food consumption of the animals and their body weight were monitored. At 80 days, oral glucose tolerance test (OGTT) was performed. At 90 days, all animals were submitted to tests, for evaluation of anxiety level(elevated plus-maze) working memory (30 sec) and long-term (24h) (inhibitory avoidance test). At 110 days, there was euthanasia and the biometric parameters were evaluated. The normocaloric diet and physical training performed by the F0 generation promoted a lower accumulation of fat in the offspring, male and female from F1 generation, compared to CSed1 (retroperitoneal fat: 37.7% in females and 27.6% in males, perigonadal fat 28.16%, in males). Differently from what happened in the F1generation, the males of the DSed2 group presented a higher accumulation of perigonadal fat, 19.4%, when compared to the group Csed2. Additionally, the protective effect of physical training in relation to the lower accumulation of retroperitoneal and perigonadal fats in the F2 generation occurred only in the DEx2 group and in the males, with a reduction of 21% and 26.8%, respectively, in relation to the DSed2 group. Females of the DSed groups of the F1 and F2 generations were not intolerant to glucose, however, there was a 11.2% reduction in the glycemia of the females of the DEx1 group when compared to the DSed1 group. In contrast to what happened in the first-generation females, males from the DSed1 group were intolerant to glucose, with an increase in blood glucose by 18.45% when compared to the CSed1 group. The group DEx1 and DEx2 had a reduction in blood glucose of 18.45% and 24.75% when compared to the DSed group. The HS / HF diet consumed by the F0 generation reduced the long-term memory of the females of the DSed2 group by 88.6% when compared to the CSed2 group. It also increased the anxiety levels of male F1 generation from the DSed1 group in relation to the CSed1 and DEx1 groups. The HS / HF diet increased the anxiety level of the F1 generation males and caused long-term memory injury in females of the F2 generation, in addition to increasing the glycemia of the first-generation diet group males and causing higher fat accumulation In the F2 generation. Physical training had a protective effect on offspring glycemia, reducing the adiposity of male and female F1 pups (control group). This effect was only maintained in the F2 generation in the male offspring of the diet group. The HS / HF diet consumed by females from weaning to lactation alters metabolism, memory and anxiety levels in the F1 and F2 generations, particularly among males. Physical training of moderate to intense intensity performed by the F0 generation protects the progeny.
Bouarab, Chloe. "Modifications post-traductionnelles des histones au sein du circuit hippocampo-amygdalien déterminant le passage d'une mémoire de peur normale à une mémoire traumatique." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0261/document.
Full textMemory alterations associated with post-traumatic stress disorder (PTSD) are a fundamental feature of this pathology. PTSD is characterized both by hypermnesia for simple salient trauma-related stimuli and amnesia for peri-traumatic contextual cues. In humans, this disorder is associated with hippocampal hypofunction and amygdalar hyperfunction, which may underlie such paradoxical memory pattern. However, neurobiological bases of PTSD, particularly at the molecular level, remain largely unknown. A behavioral model based on aversive conditioning was developed in mice by our team. This model allows the comparison between a normal, i.e. “contextualized” and adaptive, fear memory, and a PTSD-like pathological fear memory, i.e. “decontextualized” and focused on a salient cue of the trauma. Since specific epigenetic alterations have been involved in the development of contextual fear memory, our aim was the identification of the alterations in post-translational histone modifications underlying the development of traumatic memory instead of normal fear memory. Our results first reveal that normal and PTSD-like fear memory are associated with distinct acetylation/methylation profiles of histone H3 in the hippocampal-amygdalar network. Specifically, we show that, compared to normal fear memory, PTSD-like memory is associated with a switch from H3K9 hyperacetylation (marker of transcriptional activation) to H3K9 hypermethylation (marker of transcriptional repression) in hippocampal CA1, as well as a significant reduction of H3K27 trimethylation, which results in an increased transcription, in the lateral amygdala. Second, we show that the pharmacological manipulation of the acetylation/methylation balance of H3K9 in the hippocampus can prevent or promote the development of PTSD-like memory. Finally, a last series of experiments shows that (i) prenatal stress is a risk factor for the development of PTSD-like memory, (ii) which is associated with specific epigenetic alterations and (iii) that such vulnerability to stress can be transmitted to subsequent generations
Rabiei, Far Parisa. "Differential gene expression profiling of chromatin-modifying enzymes and remodeling factors in the rat motor cortex after motor skill training." Thesis, Örebro universitet, Institutionen för naturvetenskap och teknik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-28572.
Full textIstaces, Nicolas. "Transcriptional control of innate memory CD8+ T cells." Doctoral thesis, Universite Libre de Bruxelles, 2019. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/295204.
Full textDoctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
Eymard, Eric D. "Role of ETS-1 and Histone Methylation Patterns in Rapid Recall Ability of Memory T Cells." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1613744260170862.
Full textCassel, Raphaelle. "Impact de la réactivation de l'acétylation des histones sur les performances mnésiques dans un modèle transgénique murin de la maladie d'Alzheimer : vers une nouvelle stratégie thérapeutique ?" Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ040/document.
Full textAlzheimer’s disease (AD) is characterized by a progressive loss of memory and cognitive functions associated with the development of neurofibrillary tangles (NFTs) and amyloid plaques in the brain. Nowadays, there is no satisfactory cure for AD. The discovery of epigenetic alterations in AD brain led the scientist community to think about new therapeutic options. Such modifications, and notably those on histone acetylation of the chromatin, could be associated with the genetic dysfunctions observed in AD. The reestablishment of proper epigenetic regulations, and thus gene expression, appears as an original therapeutic option. Using THY-Tau22 mice, we assessed the effect of two strategies aimed at increasing histone acetylation with a HAT activator (CSP-TTK21) or an HDAC inhibitor (phenylbutyrate). We show that both therapeutic strategies allow the rescue of spatial memory performances in the THY-Tau22 mouse model. These results open new leads for AD therapeutics and research
Gully, Kay. "The plant immune system : induction, memory and de-priming of defense responses by endogenous, exogenous and synthetic elicitors." Thesis, Angers, 2019. http://www.theses.fr/2019ANGE0001/document.
Full textAs sessile organism, plants have to react quickly and strongly with defense responses to repel any invading pathogen. The plant immune system can be triggered by exogenous or endogenous elicitor molecules. Another class of elicitors are defense promoting compounds which are also known as synthetic elicitors. Here I describe the discovery and characterization of a novel family of potentially secreted small endogenous peptides (PROSCOOP) which members harbor small peptides (SCOOPs). I show that the SCOOP family is involved in plant defense and root development. Various SCOOP peptides induce short- and long-term defense responses. Moreover, treatments with the SCOOP12 peptide induce the resistance against Pseudomonas syringae in Arabidopsis. In the second part of this thesis, I show that treatments with a synthetic elicitor can lead to long-term transcriptional memory and that subsequent challenging of such plants with an exogenous elicitor reverted this transcriptional memory. In conclusion, my thesis shows (1) how diverse the function of these elicitors can be and (2) the impact the plant defense system and its triggers have on plant development and memory
Chatterjee, Snehajyoti. "Role of lysine acetyltransferase (KAT) activation in spatial memory : a new therapeutic approach for memory related disorders such as Alzheimer’s disease." Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ092/document.
Full textCREB Binding Protein (CBP) has an intrinsic lysine acetyltransferase activity and alsofunctions as a transcriptional co-activator. Both the acetyltransferase activity and the transcriptional co-activator function are critical for long-term memory formation. Importantly, CBP dysregulation has been observed in neurodegenerative conditions like in Alzheimer’s disease and Huntington’s disease. The focus of my thesis was to study the role of CBP and its activation by a new pharmacological tool, in the context of spatial memory formation, a form of memory that is very early dismantled in AD. Data obtained from my thesis clearly suggests that activation of CBP acetyltransferase function by small molecule activator CSP-TTK21 can improve memory related processes in healthy adult mice and also in a mouse model of AD, (THY-Tau22). Therefore, the strategy of pharmacological activation of CBP acetyltransferase activity has tremendous potential for use as therapeutics for the treatment of diseases related to memory impairment such as Alzheimer’s disease
Petsophonsakul, Petnoi. "Hippocampal plasticity underlying learning and memory processes in healthy and diseased conditions." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30009.
Full textThroughout life, environmental challenges promote long-lasting changes within the brain that can affect cognitive function, as well as the development of brain disorders. Within the brain, the hippocampus plays a key role in learning and memory processes. In the first study, we demonstrate how neuronal activity triggered by the learning and memory enhances the synaptic integration of adult-born hippocampal neurons that could support hippocampal function. In the second study, we show that enriched environment prevents age-related memory deficits and induces epigenetic modifications in both healthy and Alzheimer's disease conditions. This suggests that long-lasting epigenetic regulations may participate in sustaining the promnesic effects of environmental enrichment. Altogether, this thesis provides evidence of activity-dependent plasticity in the hippocampus in healthy and diseased brain, and suggests that stimulating such plasticity may contribute to improve pathological conditions
Blank, Martina. "Regulação epigenética na formação da memória aversiva : modulação via inibidores de histona desacetilases." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/119754.
Full textThe chromatin state directly impacts gene expression triggered by memory formation. Therefore, this process is of great interest to the biomedical area. Critical regulators of chromatin state and gene transcription are the epigenetic modifications such as DNA methylation and posttranslational modifications of histone proteins. One of the most studied postranslational modification of histones is histone acetylation. When histones are acetylated, chromatin is in a relaxed conformation allowing gene expression. Lysine acetylation is catalyzed by histone acetyltransferases (HATs) and is reversed by the action of histone deacetylases (HDACs). The use of histone deacetylase inhibitors (HDACis) is helping to elucidate genetic mechanisms of learning and memory. Our work is based on the hypothesis that HDACs activity is crucial for inhibitory avoidance (IA) learning responses modulation and the idea that histone acetylation is an essential step. The data presented in this work demonstrate that infusion of Trichostatin A (TSA) or Sodium Butyrate (NaB) intrahipocampally produced memory enhancement. Moreover, TSA showed two waves of memory enhancing effects when given immediately or 3 h after training coinciding with the observed waves of protein synthesis and PKA activation for memory formation. Our study also demonstrates that the enhancement of IA memory consolidation depends on the integrity of basolateral amygdala (BLA) since its functional inactivation by muscimol (MUS) completely blocked the enhancing effect of TSA infused in the rat hippocampus. Here, we also demonstrate that intraperitoneal administration of NaB immediately after training led to memory enhancement in aged rats with no cognitive deficit. Surprisingly, NaB had no effect in younger rats with normal memory retention. Finally, data presented here also demonstrate that TrkB activity in the hippocampus is crucial for long-term memory (LTM) since administration of a TrkB receptor antagonist, ANA-12, in the dorsal hippocampus immediately after training or retrieval led to memory retention impairment. Moreover, infusion of NaB before training prevented this impairing effect of TrkB antagonism. Taken together, these results show that epigenetic modulation by HDACs activity is required for memory formation. Our data also supports the idea of HDACs playing critical roles in learning and memory interacting with intracellular signaling pathways triggered by these processes.
Valiati, Fernanda Endler. "Papel das histonas deacetilases na amígdala basolateral na modulação da memória emocional." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/143055.
Full textIntroduction: Memory formation involves changes in the expression of neuronal genes. Epigenetic remodeling of chromatin and reversible post-translational modifications in the DNA or in the histone proteins represent central mechanisms in the regulation of gene expression during brain development and early learning or memory retrieval. Imbalances in the levels of histone acetylation are associated with a wide variety of brain disorders. Histone deacetylases (HDACs) play a key role in homeostasis of histone acetylation and regulation of fundamental cellular activities, such as transcription, making them a focus of study. Evidences shows that the administration of histone deacetylases inhibitors (HDACis) restore the memory associated with the regulation of gene expression and improves memory in rats. Studies in animal models have shown that memory formation involves a series of biochemical changes in several areas of the central nervous system, which the hippocampus and basolateral amygdala (BLA) are the most highlighted. In this context, experimental drugs, such as trichostatin A (TSA), that act on epigenetic mechanisms, have recently been proposed as potential therapies for the treatment of memory and cognitive dysfunction associated with psychiatric and neurological disorders. Objective: In this work we aimed to understand and elucidate the role of histone acetylation in processes involved in memory modulation using the drug TSA and is based on the hypothesis that HDACs activity is essential for the modulation of learning answers in the inhibitory avoidance (IA) task. Methods: Wistar rats were cannulated bilaterally in the amygdala. The effects of TSA micro-infusions into the BLA were observed in the consolidation and extinction of memory after training in the inhibitory avoidance task and the levels of brain-derived neurotrophic factor (BDNF) in the BLA and hippocampus related to memory consolidation. Results: The results demonstrated that the TSA infusion into BLA 1.5 h , 3 h and 6 h posttraining in the inhibitory avoidance task results in improved long-term memory (LTM). TSA accelerated the extinction of memory when infused immediately post-test. In addition, increased levels of BDNF in the hippocampus. Conclusion: These results indicate that epigenetic events play an important role in learning and memory by HDAC activity.
Rocha, Kellen Mariane Athaide. "Efeito neuroprotetor do ácido hidroxâmico de suberoilanilida (Saha), um inibidor de HDAC, em modelo de doença de Alzheimer induzida por injeção do peptídeo β-amilóide 1-42." Universidade Federal do Pampa, 2017. http://dspace.unipampa.edu.br:8080/jspui/handle/riu/3369.
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A doença de Alzheimer (DA) é uma desordem neurodegenerativa crônica caracterizada clinicamente pela perda progressiva de função cognitiva, distúrbios neuropsiquiátricos e comportamentais. Patologicamente esta doença caracteriza-se pelo acúmulo anormal do peptídeo β-amilóide (Aβ) no córtex e no hipocampo, emaranhados neurofibrilares intracelulares formados por tau hiperfosforilada, disfunção progressiva sináptica e, posteriormente perda neuronal. As opções terapêuticas disponíveis melhoram os sintomas, mas não impedem a progressão da doença, portanto, ainda está faltando uma estratégia terapêutica efetiva para DA. Há estudos relacionados à utilização de terapia epigenética para o tratamento da DA, a terapêutica mais desenvolvida é a que envolve a classe dos inibidores das deacetilases (HDACs). Assim, este trabalho tem por objetivo investigar o efeito protetor do inibidor da HDAC ácido hidroxâmico de suberoilanilida (SAHA) em um modelo de DA em camundongos. Para isso, foram utilizados 50 camundongos Swiss adultos, pesando entre 30-35 g, divididos em dois experimentos. No primeiro, os camundongos foram divididos em 6 grupos que receberam uma injeção de Aβ1-42 via intracerebroventricular (i.c.v.) no início da experiência (exceto o grupo Sham que foi utilizado como controle) para investigar a atividade das histonas acetiltransferase (HATs) e HDAC, determinação dos níveis do fator neurotrófico derivado do cérebro (BDNF), expressão do mRNA de BDNF e modulação da via (cAMP/PKA/CREB) em uma curva de tempo (6 horas, 1, 3, 7 e 21 dias). Ao final de cada tempo, os animais foram submetidos ao teste cognitivo e foram eutanasiados. O córtex pré-frontal e o hipocampo foram removidos para posteriores análises. No segundo experimento, os camundongos foram dividos em 4 grupos: Grupo Controle (sham+veículo); Grupo Aβ1-42 (Aβ1-42 + veículo); Grupo SAHA (25 mg/kg, via intraperitoneal) (sham + SAHA); Grupo Interação (Aβ1-42 + SAHA). O peptídeo Aβ1-42 ou o veículo foram infundidos por injeção i.c.v. e, um dia depois, iniciou-se o tratamento, por via i.p., durante 21 dias. Ao final do experimento os animais foram submetidos ao teste cognitivo, eutanásiados para retirada das estruturas cerebrais. As amostras foram utilizadas para a determinação dos níveis de BDNF, expressão do mRNA de BDNF, atividade enzimática das histonas (HDAC e HATs) e regulação da via cAMP/PKA/CREB. O presente estudo observou deficiências significativas causadas pela Aβ1-42 na memória (Labirinto Aquático de Morris), bem como causou desequilíbrio das enzimas HAT/HDAC, redução de cAMP, PKA e CREB e BDNF no córtex pré-frontal e hipocampo de camundongos. A inibição de HDAC, com SAHA demostrou neuroproteção nas alterações comportamentais e neuroquímicas induzidas por Aβ1-42. Estes dados mostram que a acetilação através da inibição do HDAC, desempenha um papel fundamental na mediação da memória e demonstra que SAHA poderá ser uma ferramenta médica promissora na abordagem terapêutica para o tratamento da DA.
Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized clinically by the progressive loss of cognitive function, neuropsychiatric and behavioral disorders. Pathologically this disease is characterized by the abnormal accumulation of β-amyloid peptide (Aβ) in the cortex and hippocampus, intracellular neurofibrillary tangles formed by hyperphosphorylated tau, progressive synaptic dysfunction and, later, neuronal loss. The available therapeutic options improve the symptoms, but they do not prevent the progression of the disease, therefore, an effective therapeutic strategy for AD is still lacking. There are studies related to the use of epigenetic therapy for the treatment of AD, the most developed therapy is that involving the class of deacetylase inhibitors (HDACs). Thus, this work aims to investigate the protective effect of the HDAC inhibitor hydroxamic acid suberoilanilide (SAHA) in an AD model in mice. For this, 50 Swiss adult mice weighing between 30-35 g were used, divided in two experiments. In the first, the mice were divided into 6 groups that received an injection of Aβ1-42 via the intracerebroventricular (i.c.v.) at the beginning of the experiment (except the Sham group that was used as control) to investigate histone activity acetyltransferase (HATs) and HDAC, determination of brain derived neurotrophic factor (BDNF) levels, expression of BDNF mRNA and modulation of the pathway (cAMP / PKA / CREB) in a time curve (6 hours, 1, 3, 7 and 21 days). At the end of each time, the animals were submitted to the cognitive test and were euthanized. The prefrontal cortex and hippocampus were removed for further analysis. In the second experiment, the mice were divided into 4 groups: Control Group (sham + vehicle); Group Aβ1-42 (Aβ1-42 + vehicle); SAHA group (25 mg / kg, intraperitoneal route) (sham + SAHA); Interaction Group (Aβ1-42 + SAHA). The Aβ1-42 peptide or vehicle was infused by i.c.v. and one day later the treatment was started i.p. for 21 days. At the end of the experiment the animals were submitted to the cognitive test, euthanasia for removal of the cerebral structures. The samples were used for the determination of BDNF levels, expression of BDNF mRNA, histone enzymatic activity (HDAC and HATs) and regulation of the cAMP / PKA / CREB pathway. The present study observed significant deficiencies caused by Aβ1-42 in memory (Morris Aquatic Labyrinth), as well as caused imbalance of HAT / HDAC enzymes, cAMP, PKA and CREB and BDNF reduction in the prefrontal cortex and hippocampus of mice. Inhibition of HDAC with SAHA demonstrated neuroprotection in behavioral and neurochemical changes induced by Aβ1-42. These data show that acetylation through inhibition of HDAC plays a key role in memory mediation and demonstrates that SAHA may be a promising medical tool in the therapeutic approach to AD.
Perchermeier, Sophie [Verfasser], da Costa Clarissa [Akademischer Betreuer] Prazeres, Silvia [Gutachter] Lobmaier, da Costa Clarissa [Gutachter] Prazeres, and Percy A. [Gutachter] Knolle. "Chronic Schistosoma mansoni Infection during Pregnancy: Effects on Offspring’s T Cell Differentiation Capacity, Epigenetics and Memory T Cell Compartment / Sophie Perchermeier ; Gutachter: Silvia Lobmaier, Clarissa Prazeres da Costa, Percy A. Knolle ; Betreuer: Clarissa Prazeres da Costa." München : Universitätsbibliothek der TU München, 2021. http://d-nb.info/1230061045/34.
Full textGour-ShenqKao and 高國勝. "The memory-associated alterations in protein and epigenetic signature." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/54518899760100306195.
Full text國立成功大學
基礎醫學研究所
100
The formation of long term memories requires de novo protein synthesis shortly after the relevant experience. Two-dimensional gel electrophoresis was used to identify accumbal candidate proteins involved in the retrieval of a cue-mediated memory. Among the identified candidate proteins, a downregulated 14-3-3ζ protein was chosen and confirmed by Western immunoblotting. A polymer-mediated plasmid DNA delivery system was then used to overexpress 14-3-3ζ protein in the mouse nucleus accumbens before the CPP retrieval tests. Overexpression of accumbal 14-3-3ζ protein was found to diminish conditioned cue/context-mediated cocaine-induced CPP. Overexpression of accumbal 14-3-3ζ protein did not produce motor activity-impairing effect or alter local dopamine metabolism. Moreover, overexpression of accumbal 14-3-3ζ protein did not affect food-induced CPP. These results indicated that overexpressed accumbal 14-3-3ζ protein specifically decreased conditioned cue/context-mediated cocaine memory. In addition, epigenetic processes influence stress effects of early-life experience on learning and memory. In this study, a fear-potentiated startle was used to model the acquisition of traumatic event-related memory in female rats experiencing early life stress. We found that a 1 hr/day maternal and sibling separation throughout day 2-9 postpartum (D2-9PP) caused a decrease in the fear-potentiated startle, but not acoustic startle baseline, in female adult rats. The separation procedure did not affect baseline and acute stress-stimulated corticosterone (CORT) secretion but produced an increase in serum estradiol concentration. Moreover, the separation procedure did not affect histone 3 lysine 9 (H3K9) acetylation but decreased H3K9 mono- and tri-methylation in frontal cortices. Treatment with 5-aza-2’-deoxycytidine (AZA), an H3K9 acetylation enhancer, at 2 variant dosing regimens did not affect the separation-decreased fear-potentiated startle. Treatment with valproic acid (VPA), a histone deacetylase inhibitor, at 3 dosing regimens prior to daily separation reversed such a decrease in fear-potentiated startle. An effective VPA dosing regimen did not affect early life separation-produced increase in serum E2 secretion but reversed separation-decreased H3K9 mono- and tri-methylation in frontal cortices. Eight consecutive days of VPA and AZA treatments starting at D28PP were ineffective in altering the separation-decreased fear-potentiated startle, -increased E2 concentration, or -decreased frontal cortical mono-, tri-methylation. We suggest that decreased H3K9 mono- and tri-methylation in frontal cortex may be involved in early life separation-decreased fear memory formation. Early, but not late, VPA treatment is effective in treating early life stress-produced decrease in cued fear conditioning.
Balta, Ana-Maria. "Epigenetic effects of learning and memory in the I-Ppo-I mouse." Thesis, 2016. https://hdl.handle.net/2144/19201.
Full textSIMANULLANG, BASTA, and 司峇塔. "The investigation of the epigenetic modification regulated mi-RNA induction in the hippocampus after spatial learning and memory formation." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/6n7xxg.
Full text國立中央大學
生命科學系
107
Behavior is driven by environmental stimulation that triggers brain activity with lots of molecular mechanisms. The process of learning and memory contains stimulation-induced changes that happen in the synaptic connections between neurons in the hippocampus, which plays a pivotal role in the formation of long term somatic and episodic memories. By Morris water maze experiment and RNA analysis, we show that some micro-RNAs (miRNA) are expressed differently between learned and unlearned mice. One of the miRNAs, miR-466f-3p, which belongs to post transcriptional regulator, is abundantly express in brain and generated in the intron-10 of Sfmbt2 gene. However, the mRNA expression of Sfmbt2 is significantly different from miR-466f-3p. Inhibition of epigenetic modification, such as DNA methylation, can affect gene expression. Treatment of 5’Aza-dC, a methyltransferase inhibitor, to the hippocampal primary culture neuron causes Bdnf, Nrf2, Sfmbt2 mRNA and miR466f-3p expression increased. However, the methylation pattern in the promoter region of the miR-466f cluster is not significantly different between learned and unlearned mice. The evidence show that the changes of DNA methylation under the stress of the Morris water maze indirectly participate in the regulating of miR-466f-3p induction in the hippocampus-dependent spatial learning and memory formation. Keywords: Epigenetic, mi-RNAs induction, Methylation
Pinc, Jan. "Vznik, přenos a ekologický význam apomixie v rodě Hieracium s.str.: role genetických a epigenetických mechanismů." Doctoral thesis, 2020. http://www.nusl.cz/ntk/nusl-436152.
Full textAl-Rikabi, Aaiad H. A., Desmond J. Tobin, Kirsten Riches-Suman, and M. Julie Thornton. "Dermal fibroblasts cultured from donors with type 2 diabetes mellitus retain an epigenetic memory associated with poor wound healing responses." 2020. http://hdl.handle.net/10454/18438.
Full textThe prevalence of Type 2 diabetes mellitus (T2DM) is escalating globally. Patients suffer from multiple complications including the development of chronic wounds that can lead to amputation. These wounds are characterised by an inflammatory environment including elevated tumour necrosis factor alpha (TNF-α). Dermal fibroblasts (DF) are critical for effective wound healing, so we sought to establish whether there were any differences in DF cultured from T2DM donors or those without diabetes (ND-DF). ND- and T2DM-DF when cultured similarly in vitro secreted comparable concentrations of TNF-α. Functionally, pre-treatment with TNF-α reduced the proliferation of ND-DF and transiently altered ND-DF morphology; however, T2DM-DF were resistant to these TNF-α induced changes. In contrast, TNF-α inhibited ND- and T2DM-DF migration and matrix metalloprotease expression to the same degree, although T2DM-DF expressed significantly higher levels of tissue inhibitor of metalloproteases (TIMP)-2. Finally, TNF-α significantly increased the secretion of pro-inflammatory cytokines (including CCL2, CXCL1 and SERPINE1) in ND-DF, whilst this effect in T2DM-DF was blunted, presumably due to the tendency to higher baseline pro-inflammatory cytokine expression observed in this cell type. Collectively, these data demonstrate that T2DM-DF exhibit a selective loss of responsiveness to TNF-α, particularly regarding proliferative and secretory functions. This highlights important phenotypic changes in T2DM-DF that may explain the susceptibility to chronic wounds in these patients.
This study was funded by an Iraqi government studentship to AHAA-R.
"The Dirty Joke of Cyberpunk or the Humanism of Posthumanism in the Cyberpunk Tradition: Epigenetic Memory and Technology in Gibson's Neuromancer and Stephenson's Snow Crash." Master's thesis, 2013. http://hdl.handle.net/2286/R.I.17778.
Full textDissertation/Thesis
M.A. English 2013
Löns, Sebastian. "Epigenetik in der Schizophrenie und der Einfluss von Histon-Deacetylasen auf die Arbeitsgedächtnisfunktion." Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0023-963D-C.
Full textGanguly, Diep. "Training Memory: Exploring the Intersection of Plant Stress Signalling and DNA Methylation." Phd thesis, 2018. http://hdl.handle.net/1885/145958.
Full textStilling, Roman. "The role of Kat2a during memory formation and chromatin plasticity in the aging murine hippocampus." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0001-BAC5-2.
Full textBrazão, João António Lima de Andrade Conde. "Relatório de estágio e monografia intitulada :"mecanismos epigenéticos na formação de memória e capacidades cognitivas"." Master's thesis, 2017. http://hdl.handle.net/10316/83661.
Full textA habilidade do organismo humano em adaptar o seu comportamento em resposta a estímulos ambientais ao longo do tempo, fundamenta-se na plasticidade estrutural e funcional do SNC. É atualmente conhecido que os processos em torno da memória celular (diferenciação), e da memória neurológica têm similaridades, não só ao nível da sua génese como também da sua regulação, orquestrada por mecanismos epigenéticos. A definição molecular moderna de epigenética consiste no conjunto de alterações na estrutura base da cromatina que, coletivamente, originam e propagam diferentes padrões de expressão de genes, transcrição, e silenciamento em relação ao mesmo genoma que não são explicados por mudanças na sequência de DNA. Marcas epigenéticas como a metilação do DNA e modificações pós-tradução das histonas têm vindo a comprovar-se cada vez mais como imprescindíveis reguladores dos processos de memória. As suas funções de regulação dinâmica da transcrição de genes em resposta à ativação neuronal mostram-se relevantes e influentes no processo de formação de memória. A natureza persistente, mesmo após divisão celular, de mecanismos como a metilação do DNA sugere também a existência de um papel da epigenética na manutenção da memória previamente formada. O conteúdo da presente monografia tem como foco a ligação entre determinados processos envolvidos na formação e manutenção de memória e capacidades cognitivas, compreendendo vias de sinalização comuns a ambos os tipos de memória referidos, e os mecanismos epigenéticos implicados na regulação desses mesmos processos e consequentes respostas, dependentes de uma articulação e encadeamento com um elevado nível de precisão temporal e especificidade.
The ability of the human organism to adapt its behavior in response to environmental stimuli through time is based on the structural and functional plasticity of the CNS. It is known that the processes regarding cellular memory (differentiation) and neurological memory have similarities, not only on the level of their genesis but of their regulation as well, orchestrated by epigenetic mechanisms. The modern molecular definition of Epigenetics comprehends the range of modifications in the basic chromatin structure that, collectively, originate and spread different gene expression patterns, transcription and silencing in relation to the same genome that are not explained by changes in the DNA sequence. Epigenetic tags like DNA methylation and histone post-translational modifications have been increasingly seen as crucial regulators of memory processes. Their functions of dynamic regulation of gene transcription in answer to the neuronal activation have been shown to be relevant and influential in memory formation. The persistent nature of mechanisms like DNA methylation, even after cell division, also suggests the existence of a role to epigenetics on the maintenance of previously formed memory. The content of the present monography spotlights the connection of particular processes involved in the formation and maintenance of memory and cognition, including signaling pathways common to both types of memory (cellular and neuronal) and the epigenetic mechanisms implicated on the regulation of these same processes and subsequent outcomes, dependent of an articulation and sequencing comprising a high level of temporal precision and specificity.
Urban, Inga. "The Role of Lysine Acetyltransferase Tip60 in the Murine Hippocampus." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0022-6046-5.
Full textShomroni, Orr. "Development of algorithms and next-generation sequencing data workflows for the analysis of gene regulatory networks." Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-0023-3E0C-8.
Full textRajput, Ashish. "Using cell type-specific methods to understand molecular processes in the brain." Doctoral thesis, 2018. http://hdl.handle.net/11858/00-1735-0000-002E-E63D-B.
Full textNavarro, Sala Magdalena. "Changes in gene expression linked to Alzheimer's disease and "healthy" cognitive aging." Doctoral thesis, 2018. http://hdl.handle.net/11858/00-1735-0000-002E-E59C-E.
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