Relevant bibliographies by topics / Memory Methylene blue. Brain

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Academic literature on the topic 'Memory Methylene blue. Brain'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Memory Methylene blue. Brain"

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Callaway, Narriman Lee, Penny D. Riha, Aleksandra K. Bruchey, Zeenat Munshi, and F. Gonzalez-Lima. "Methylene blue improves brain oxidative metabolism and memory retention in rats." Pharmacology Biochemistry and Behavior 77, no. 1 (January 2004): 175–81. http://dx.doi.org/10.1016/j.pbb.2003.10.007.

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Riha, Penny D., Aleksandra K. Bruchey, David J. Echevarria, and F. Gonzalez-Lima. "Memory facilitation by methylene blue: Dose-dependent effect on behavior and brain oxygen consumption." European Journal of Pharmacology 511, no. 2-3 (March 2005): 151–58. http://dx.doi.org/10.1016/j.ejphar.2005.02.001.

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Mori, Takashi, Naoki Koyama, Tatsuya Segawa, Masahiro Maeda, Nobuhiro Maruyama, Noriaki Kinoshita, Huayan Hou, Jun Tan, and Terrence Town. "Methylene Blue Modulates β-Secretase, Reverses Cerebral Amyloidosis, and Improves Cognition in Transgenic Mice." Journal of Biological Chemistry 289, no. 44 (August 25, 2014): 30303–17. http://dx.doi.org/10.1074/jbc.m114.568212.

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Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in the brains of patients with Alzheimer disease (AD). Here, we tested whether the experimental agent methylene blue (MB), used for treatment of methemoglobinemia, might improve AD-like pathology and behavioral deficits. We orally administered MB to the aged transgenic PSAPP mouse model of cerebral amyloidosis and evaluated cognitive function and cerebral amyloid pathology. Beginning at 15 months of age, animals were gavaged with MB (3 mg/kg) or vehicle once daily for 3 months. MB treatment significantly prevented transgene-associated behavioral impairment, including hyperactivity, decreased object recognition, and defective spatial working and reference memory, but it did not alter nontransgenic mouse behavior. Moreover, brain parenchymal and cerebral vascular β-amyloid deposits as well as levels of various Aβ species, including oligomers, were mitigated in MB-treated PSAPP mice. These effects occurred with inhibition of amyloidogenic APP proteolysis. Specifically, β-carboxyl-terminal APP fragment and β-site APP cleaving enzyme 1 protein expression and activity were attenuated. Additionally, treatment of Chinese hamster ovary cells overexpressing human wild-type APP with MB significantly decreased Aβ production and amyloidogenic APP proteolysis. These results underscore the potential for oral MB treatment against AD-related cerebral amyloidosis by modulating the amyloidogenic pathway.
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Sadovnikova, Irina S., Artem P. Gureev, Daria A. Ignatyeva, Maria V. Gryaznova, Ekaterina V. Chernyshova, Ekaterina P. Krutskikh, Anastasia G. Novikova, and Vasily N. Popov. "Nrf2/ARE Activators Improve Memory in Aged Mice via Maintaining of Mitochondrial Quality Control of Brain and the Modulation of Gut Microbiome." Pharmaceuticals 14, no. 7 (June 23, 2021): 607. http://dx.doi.org/10.3390/ph14070607.

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Aging is one of the most serious factors for central nervous dysfunctions, which lead to cognitive impairment. New highly effective drugs are required to slow the development of cognitive dysfunction. This research studied the effect of dimethyl fumarate (DMF), methylene blue (MB), and resveratrol (RSV) on the cognitive functions of 15-month-old mice and their relationship to the maintenance of mitochondrial quality control in the brain and the bacterial composition of the gut microbiome. We have shown that studied compounds enhance mitochondrial biogenesis, mitophagy, and antioxidant defense in the hippocampus of 15-month-old mice via Nrf2/ARE pathway activation, which reduces the degree of oxidative damage to mtDNA. It is manifested in the improvement of short-term and long-term memory. We have also shown that memory improvement correlates with levels of Roseburia, Oscillibacter, ChristensenellaceaeR-7, Negativibacillus, and Faecalibaculum genera of bacteria. At the same time, long-term treatment by MB induced a decrease in gut microbiome diversity, but the other markers of dysbiosis were not observed. Thus, Nrf2/ARE activators have an impact on mitochondrial quality control and are associated with a positive change in the composition of the gut microbiome, which together lead to an improvement in memory in aged mice.
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Lummus, Seth, and Bette Kay Kleinschmidt-DeMasters. "Methylene Blue “Avatar” Brain." Journal of Neuropathology & Experimental Neurology 72, no. 3 (March 2013): 263–65. http://dx.doi.org/10.1097/nen.0b013e318283d41a.

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Gonzalez-Lima, F. "Extinction Memory Improvement by the Metabolic Enhancer Methylene Blue." Learning & Memory 11, no. 5 (September 1, 2004): 633–40. http://dx.doi.org/10.1101/lm.82404.

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R. Suryawanshi, Chandani, and Vinod Nayyar. "BLUE BRAIN." INTERNATIONAL JOURNAL OF MANAGEMENT & INFORMATION TECHNOLOGY 7, no. 2 (November 30, 2013): 1009–17. http://dx.doi.org/10.24297/ijmit.v7i2.3294.

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Today scientists are in research to create an artificial brain that can think, respond, take decision, and keep anything in memory. The main aim is to upload human brain into machine. So that man can think, take decision without any effort. After the death of the body, the virtual brain will act as the man. So, even after the death of a person we will not loose the knowledge, intelligence, personalities, feelings and memories of that man, that can be used for the development of the human society. Technology is growing faster than every thing. IBM is now in research to create a virtual brain, called Blue brain. If possible, this would be the first virtual brain of the world. IBM, in partnership with scientists at Switzerlands Ecole Polytech- nique Federale de Lausannes (EPFL) Brain and Mind Institute will begin simulating the brains biological systems and output the data as a working 3-dimensional model that will recreate the high-speed electrochemical interactions that take place within the brains interior. These include cognitive functions such as language, learning, perception and memory in addition to brain malfunction such as psychiatric disorders like depression and autism. From there, the modeling will expand to other regions of the brain and, if successful, shed light on the relationships between genetic, molecular and cognitive functions of the brain.
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Talley Watts, Lora, Justin Alexander Long, Jonathan Chemello, Samantha Van Koughnet, Angelica Fernandez, Shiliang Huang, Qiang Shen, and Timothy Q. Duong. "Methylene Blue Is Neuroprotective against Mild Traumatic Brain Injury." Journal of Neurotrauma 31, no. 11 (June 2014): 1063–71. http://dx.doi.org/10.1089/neu.2013.3193.

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Haouzi, Philippe, Takashi Sonobe, and Annick Judenherc-Haouzi. "Hydrogen sulfide intoxication induced brain injury and methylene blue." Neurobiology of Disease 133 (January 2020): 104474. http://dx.doi.org/10.1016/j.nbd.2019.05.013.

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Lee, Yong Soo, and Robert D. Wurster. "Methylene blue induces cytotoxicity in human brain tumor cells." Cancer Letters 88, no. 2 (January 1995): 141–45. http://dx.doi.org/10.1016/0304-3835(94)03629-w.

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Dissertations / Theses on the topic "Memory Methylene blue. Brain"

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Edlin, Shaun Michael. "Methylene blue, spatial memory and anterior thalamic lesions relevant to amnesic disorders." Thesis, University of Canterbury. Psychology, 2011. http://hdl.handle.net/10092/6521.

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While recent studies have focused on methylene blue’s interaction with amyloid plaques and neurofibrillary tangles in Alzheimer’s disease,!no studies have investigated the efficacy of methylene blue in animal-lesion models of regional pathology relevant to AD. The goal of this dissertation was to examine the effects of methylene blue on spatial memory in aged Wistar rats with lesions to the anterior thalamic nuclei (ATN), part of an extended episodic memory system that shows early pathology in AD and diencephalic amnesia. First, 12 ATN rats were compared to 14 aged shams (18 to 22 months old) to assess spatial memory acquisition in a standard water maze task (10 days). Rats in each group then received intraperitoneal injections of methylene blue (1 mg/kg) or placebo 1 hour after each daily trial for 10 days in which acquisition of a new platform position was examined, followed by a probe trial 5 days later. Anterior thalamic lesions impaired initial acquisition of the reference memory task. In the subsequent acquisition and probe trial, methylene blue treatment vs. placebo improved spatial learning in ATN rats, but there was no effect in sham rats. These results provide the first evidence that methylene blue may prevent the learning impairments observed in rats with lesions to the anterior thalamus and supports methylene blue as a potential therapeutic intervention for older humans with memory disorders associated with injury to the ATN and the extended episodic memory system.
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Miclescu, Adriana. "Cerebral Protection in Experimental Cardiopulmonary Resuscitation With Special Reference to the Effects of Methylene Blue /." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-106831.

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Xavier, Marcelo Souza. "Efeito do azul de metileno como adjuvante no desfecho da parada cardíaca: estudo experimental em ratos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-02072018-123155/.

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INTRODUÇAO: O uso da epinefrina na ressuscitação cardiopulmonar (RCP) tem sido questionado devido aos efeitos adversos como dano miocárdico e cerebral. Fármacos como azul de metileno têm sido estudados como adjuvantes, objetivando reduzir essas lesões. OBJETIVOS: Neste estudo objetivou-se avaliar o efeito da administração do azul de metileno em bôlus durante a RCP, na lesão miocárdica e cerebral. MÉTODO: Quarenta e nove ratos Wistar machos submetidos a parada cardíaca por fibrilação ventricular foram distribuídos aleatoriamente em quatro grupos com 11 animais: azul de metileno (GA, 2mg/kg), solução salina (GC, salina 0,9% 0,1ml), epinefrina (GE, 20mcg/kg), epinefrina + azul de metileno (GM), além do grupo sham com 5 animais. A fibrilação ventricular foi induzida por estimulação elétrica direto no ventrículo direito por 3 minutos, sendo mantidos por mais 2 minutos em anóxia. As manobras de RCP foram iniciadas com o fármaco correspondente de cada grupo, massagem torácica, ventilação e desfibrilação. Após retorno a circulação espontânea (RCE), os animais foram observados durante quatro horas. Foram coletados sangue para gasometria e troponina, tecido cardíaco e cerebral para análise histológica, marcação de TUNEL, marcadores inflamatórios e de estresse oxidativo. Os grupos foram comparados por meio do teste não paramétrico de Kruskal-Wallis, com o teste de comparação múltipla com correção de Bonferroni quando adequado. RESULTADOS: Animais do grupo GE apresentaram 63% de RCE, enquanto o GC e GM obtiveram 40% e 45%, respectivamente, sem diferença estatística entre os grupos (p= 0,672). O grupo GA apresentou apenas 18% de RCE e foi excluído da análise. O tempo de RCP do GC foi maior comparado aos grupos GE e GM, mas sem diferença estatisticamente significativa. Os animais do grupo GM apresentaram PAM maior comparado ao grupo GC, no momento imediatamente após a RCE (P=0,007). Em todos os grupos os animais apresentaram acidose, queda da PaO2 e aumento do lactato após PCR e RCP. A mediana da troponina sérica foi maior no GC (130ng/ml) comparada ao grupo GE (3,8ng/ml), e GM (43,7ng/ml), porém sem diferença estatística. O grupo GC apresentou aumento significativo na expressão proteica dos marcadores BAX e TLR4. Não houve diferença estatística em relação a histologia e marcação de TUNEL entre os grupos submetidos a PCR. CONCLUSÃO: A utilização de azul de metileno em bolus na RCP de forma isolada apresentou resultados negativos em relação ao retorno da circulação espontânea. A utilização de azul de metileno associada a epinefrina não diminuiu a presença de lesões no cérebro e no coração decorrentes da parada cardíaca
INTRODUCTION: The use of epinephrine in cardiopulmonary resuscitation (CPR) has been questioned due to adverse effects such as myocardial and cerebral damage. Drugs such as methylene blue have been studied as adjuvants in order to reduce lesions. OBJECTIVES: The aim of this study was to evaluate the effect of methylene blue administration during CPR on myocardial and cerebral lesion. METHOD: Forty nine Wistar male rats submitted to ventricular fibrillation cardiac arrest (CA) were randomly assigned to four principal groups with 11 cases each one: methylene blue (MB, 2mg/kg), control (CTRL, 0.1ml saline 0.9%), epinephrine (EPI, 20?g/kg), epinephrine plus methylene blue (EPI+MB), and a sham group, wich have 5 cases. Ventricular fibrillation was induced by direct electrical stimulation in the right ventricle for 3 minutes and anoxia was maintained until a total of 5 minutes. CPR was initiated using the group drug, ventilation, chest compressions and defibrillation. The animals were observed for four hours after return of spontaneous circulation (ROSC). Blood samples were collected for blood gas and troponin measurements. Heart and brain tissues were harvested for the evaluation of oxidative stress, inflamation, histological and TUNEL staining. Groups were compared using the non-parametric Kruskal-Wallis test and Bonferroni post test. RESULTS: ROSC was achieved in 63% of the cases in EPI, 40% in CTRL, and 45% in EPI+MB (P=0.672). MB was excluded from analysis because of its low ROSC rate (18%). CPR duration was longer in CTRL compared to EPI and EPI+MB, without statistical significance. EPI+MB animals presented higher arterial pressure compared to the CTRL group, immediately after ROSC (P=0.007). All animals presented acidosis, decreased PaO2 and increased lactate after CA and CPR. Serum troponin was higher in CTRL (130ng/ml) compared with EPI (3.8ng/ml) and EPI+MB (43.7ng/ml), without statistical significance. CTRL presented higher BAX and TLR4 expression. There was no difference in TUNEL staining and histology among CA groups. CONCLUSION: Methylene blue in bolus during CPR did not improve outcome. Methylene blue combined with epinephrine did not decrease CA-related myocardial and cerebral lesions
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Wrubel, Kathryn Marigrace. "Memory improvement with the metabolic enhancer methylene blue." Thesis, 2006. http://hdl.handle.net/2152/2671.

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Bruchey, Aleksandra Krsmanović. "Metabolic mapping of rat brain activity associated with conditioned fear extinction and renewal, and improvement of extinction memory by the metabolic enhancer methylene blue." Thesis, 2006. http://hdl.handle.net/2152/2468.

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Riha, Penny Denise 1975. "Metabolic impairment of the posterior cingulate cortex and reversal by methylene blue: a novel model and treatment of early stage Alzheimer's disease." Thesis, 2007. http://hdl.handle.net/2152/3663.

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Alzheimer's disease (AD) is associated with decreased brain energy metabolism. Hypometabolism in the posterior cingulate cortex (PCC) occurs before the onset of memory deficits in subjects at genetic risk for AD who are not yet cognitively impaired. There is a specific inhibition in cytochrome oxidase (C.O.) in the PCC, an area involved in spatial navigation. Creating an animal model that exhibits the early pathophysiology of AD is important for developing and testing drugs that could reverse memory problems associated with such deficits. Methylene blue (MB) is a compound that improves C.O. activity and memory retention in rats. This dissertation had three specific aims: 1) to examine if isolated PCC hypometabolism causes spatial memory deficits in rats; 2) to find a dose of MB that improves memory without nonspecific behavioral effects; and 3) to prevent memory deficits from PCC hypometabolism with low dose MB. PCC hypometabolism was produced by focal administration of sodium azide, an inhibitor of C.O. activity. PCC hypometabolism resulted in impaired spatial memory in a hole board food-search task, increased oxidative damage, and neurotoxicity in the PCC. In addition, PCC hypometabolism resulted in reduced inter-regional correlations in brain activity. Our second set of studies examined the dose-response effects of MB. Our findings demonstrated that a low dose of MB: 1) enhanced memory in open field habituation and object recognition tasks; 2) did not affect general locomotor activity, exploration, motivation, or anxiety; and 3) increased brain oxygen consumption 24 hr after in vivo administration. Finally, our last study found that low dose MB prevented the deficits caused by PCC hypometabolism. MB did not prevent PCC inhibition or cell loss caused by sodium azide. Inter-regional correlations of brain metabolic activity suggested that rats treated with MB were using a different, but equally efficient, strategy for memory retrieval. This animal model of C.O. hypometabolism in the PCC can provide information to understand the mechanisms that regulate early pathological degeneration and reveal new therapeutic strategies aimed at reducing or preventing cognitive decline. Studies of low dose MB in humans are needed to examine its effects in AD patients.
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Book chapters on the topic "Memory Methylene blue. Brain"

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Wiklund, Lars, Aruna Sharma, Ranjana Patnaik, Dafin F. Muresanu, Seaab Sahib, Z. Ryan Tian, Rudy J. Castellani, Ala Nozari, José Vicente Lafuente, and Hari Shanker Sharma. "Upregulation of hemeoxygenase enzymes HO-1 and HO-2 following ischemia-reperfusion injury in connection with experimental cardiac arrest and cardiopulmonary resuscitation: Neuroprotective effects of methylene blue." In Nanomedicine and Neuroprotection in Brain Diseases, 317–75. Elsevier, 2021. http://dx.doi.org/10.1016/bs.pbr.2021.06.009.

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Conference papers on the topic "Memory Methylene blue. Brain"

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Stelmashook, Elena, Elizaveta Genrikhs, Svetlana Novikova, and Nickolay Isaev. "NEUROPROTECTIVE EFFECT OF METHYLENE BLUE IN TRAUMATIC BRAIN." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2336.sudak.ns2021-17/357.

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Feng, Xin, Peter Jermain, Alona Muzikansky, Alonzo Ross, Michael Hamblin, and Anna N. Yaroslavsky. "Quantifying Subcellular Localization of Methylene Blue in Cultured Brain Cells." In Frontiers in Optics. Washington, D.C.: OSA, 2019. http://dx.doi.org/10.1364/fio.2019.jtu3a.97.

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