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155 results on '"McEwen, Bruce"'

2. Moderate exercise ameliorates dysregulated hippocampal glycometabolism and memory function in a rat model of type 2 diabetes

Author

Ministry of Education, Culture, Sports, Science and Technology (Japan), Japan Society for the Promotion of Science, Shima, Takeru, Matsui, Takashi, Jesmin, Subrina, Okamoto, Masahiro, Soya, Mariko, Inoue, Koshiro, Liu, Yu-Fan, Torres-Alemán, Ignacio, McEwen, Bruce S., Soya, Hideaki, Ministry of Education, Culture, Sports, Science and Technology (Japan), Japan Society for the Promotion of Science, Shima, Takeru, Matsui, Takashi, Jesmin, Subrina, Okamoto, Masahiro, Soya, Mariko, Inoue, Koshiro, Liu, Yu-Fan, Torres-Alemán, Ignacio, McEwen, Bruce S., and Soya, Hideaki

Abstract

[Aims/hypothesis]: Type 2 diabetes is likely to be an independent risk factor for hippocampal-based memory dysfunction, although this complication has yet to be investigated in detail. As dysregulated glycometabolism in peripheral tissues is a key symptom of type 2 diabetes, it is hypothesised that diabetes-mediated memory dysfunction is also caused by hippocampal glycometabolic dysfunction. If so, such dysfunction should also be ameliorated with moderate exercise by normalising hippocampal glycometabolism, since 4 weeks of moderate exercise enhances memory function and local hippocampal glycogen levels in normal animals., [Methods]: The hippocampal glycometabolism in OLETF rats (model of human type 2 diabetes) was assessed and, subsequently, the effects of exercise on memory function and hippocampal glycometabolism were investigated., [Results]: OLETF rats, which have memory dysfunction, exhibited higher levels of glycogen in the hippocampus than did control rats, and breakdown of hippocampal glycogen with a single bout of exercise remained unimpaired. However, OLETF rats expressed lower levels of hippocampal monocarboxylate transporter 2 (MCT2, a transporter for lactate to neurons). Four weeks of moderate exercise improved spatial memory accompanied by further increase in hippocampal glycogen levels and restoration of MCT2 expression independent of neurotrophic factor and clinical symptoms in OLETF rats., [Conclusions/interpretation]: Our findings are the first to describe detailed profiles of glycometabolism in the type 2 diabetic hippocampus and to show that 4 weeks of moderate exercise improves memory dysfunction in type 2 diabetes via amelioration of dysregulated hippocampal glycometabolism. Dysregulated hippocampal lactate-transport-related glycometabolism is a possible aetiology of type-2-diabetes-mediated memory dysfunction.

Published
2017

3. A sexually dimorphic pre-stressed translational signature in CA3 pyramidal neurons of BDNF Val66Met mice.

Author

Marrocco, Jordan, Petty, Gordon H., Ríos, Mariel B., Gray, Jason D., Kogan, Joshua F., Waters, Elizabeth M., Schmidt, Eric F., Lee, Francis S., and McEwen, Bruce S.

Subjects
PYRAMIDAL neurons, GENETIC regulation, RIBOSOMES, COGNITION disorders, MICE, NUCLEOTIDE sequence
Abstract

Males and females use distinct brain circuits to cope with similar challenges. Using RNA sequencing of ribosome-bound mRNA from hippocampal CA3 neurons, we found remarkable sex differences and discovered that female mice displayed greater gene expression activation after acute stress than males. Stress-sensitive BDNF Val66Met mice of both sexes show a pre-stressed translational phenotype in which the same genes that are activated without applied stress are also induced in wild-type mice by an acute stressor. Behaviourally, only heterozygous BDNF Val66Met females exhibit spatial memory impairment, regardless of acute stress. Interestingly, this effect is not observed in ovariectomized heterozygous BDNF Val66Met females, suggesting that circulating ovarian hormones induce cognitive impairment in Met carriers. Cognitive deficits are not observed in males of either genotype. Thus, in a brain region not normally associated with sex differences, this work sheds light on ways that genes, environment and sex interact to affect the transcriptome's response to a stressor. [ABSTRACT FROM AUTHOR]

Published
2017
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4. Moderate exercise ameliorates dysregulated hippocampal glycometabolism and memory function in a rat model of type 2 diabetes.

Author

Shima, Takeru, Matsui, Takashi, Jesmin, Subrina, Okamoto, Masahiro, Soya, Mariko, Inoue, Koshiro, Liu, Yu-Fan, Torres-Aleman, Ignacio, McEwen, Bruce, and Soya, Hideaki

Abstract

Aims/hypothesis: Type 2 diabetes is likely to be an independent risk factor for hippocampal-based memory dysfunction, although this complication has yet to be investigated in detail. As dysregulated glycometabolism in peripheral tissues is a key symptom of type 2 diabetes, it is hypothesised that diabetes-mediated memory dysfunction is also caused by hippocampal glycometabolic dysfunction. If so, such dysfunction should also be ameliorated with moderate exercise by normalising hippocampal glycometabolism, since 4 weeks of moderate exercise enhances memory function and local hippocampal glycogen levels in normal animals. Methods: The hippocampal glycometabolism in OLETF rats (model of human type 2 diabetes) was assessed and, subsequently, the effects of exercise on memory function and hippocampal glycometabolism were investigated. Results: OLETF rats, which have memory dysfunction, exhibited higher levels of glycogen in the hippocampus than did control rats, and breakdown of hippocampal glycogen with a single bout of exercise remained unimpaired. However, OLETF rats expressed lower levels of hippocampal monocarboxylate transporter 2 (MCT2, a transporter for lactate to neurons). Four weeks of moderate exercise improved spatial memory accompanied by further increase in hippocampal glycogen levels and restoration of MCT2 expression independent of neurotrophic factor and clinical symptoms in OLETF rats. Conclusions/interpretation: Our findings are the first to describe detailed profiles of glycometabolism in the type 2 diabetic hippocampus and to show that 4 weeks of moderate exercise improves memory dysfunction in type 2 diabetes via amelioration of dysregulated hippocampal glycometabolism. Dysregulated hippocampal lactate-transport-related glycometabolism is a possible aetiology of type-2-diabetes-mediated memory dysfunction. [ABSTRACT FROM AUTHOR]

Published
2017
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5. Mechanisms of stress in the brain.

Author

McEwen, Bruce S, Bowles, Nicole P, Gray, Jason D, Hill, Matthew N, Hunter, Richard G, Karatsoreos, Ilia N, and Nasca, Carla

Subjects
*PHYSIOLOGICAL stress, *BRAIN research, *CELL membranes, *CYTOSKELETON, *GLUCOCORTICOIDS
Abstract

The brain is the central organ involved in perceiving and adapting to social and physical stressors via multiple interacting mediators, from the cell surface to the cytoskeleton to epigenetic regulation and nongenomic mechanisms. A key result of stress is structural remodeling of neural architecture, which may be a sign of successful adaptation, whereas persistence of these changes when stress ends indicates failed resilience. Excitatory amino acids and glucocorticoids have key roles in these processes, along with a growing list of extra- and intracellular mediators that includes endocannabinoids and brain-derived neurotrophic factor (BDNF). The result is a continually changing pattern of gene expression mediated by epigenetic mechanisms involving histone modifications and CpG methylation and hydroxymethylation as well as by the activity of retrotransposons that may alter genomic stability. Elucidation of the underlying mechanisms of plasticity and vulnerability of the brain provides a basis for understanding the efficacy of interventions for anxiety and depressive disorders as well as age-related cognitive decline. [ABSTRACT FROM AUTHOR]

Published
2015
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6. Adaptive changes in the kinetochore architecture facilitate proper spindle assembly.

Author

Magidson, Valentin, Paul, Raja, Yang, Nachen, Ault, Jeffrey G., O'Connell, Christopher B., Tikhonenko, Irina, McEwen, Bruce F., Mogilner, Alex, and Khodjakov, Alexey

Subjects
CELL cycle, KINETOCHORE, MICROTUBULES, DYNEIN, ADENOSINE triphosphatase
Abstract

Mitotic spindle formation relies on the stochastic capture of microtubules at kinetochores. Kinetochore architecture affects the efficiency and fidelity of this process with large kinetochores expected to accelerate assembly at the expense of accuracy, and smaller kinetochores to suppress errors at the expense of efficiency. We demonstrate that on mitotic entry, kinetochores in cultured human cells form large crescents that subsequently compact into discrete structures on opposite sides of the centromere. This compaction occurs only after the formation of end-on microtubule attachments. Live-cell microscopy reveals that centromere rotation mediated by lateral kinetochore-microtubule interactions precedes the formation of end-on attachments and kinetochore compaction. Computational analyses of kinetochore expansion-compaction in the context of lateral interactions correctly predict experimentally observed spindle assembly times with reasonable error rates. The computational model suggests that larger kinetochores reduce both errors and assembly times, which can explain the robustness of spindle assembly and the functional significance of enlarged kinetochores. [ABSTRACT FROM AUTHOR]

Published
2015
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9. Stress and Allostasis.

Author

Karatsoreos, Ilia N. and McEwen, Bruce S.

Abstract

The concept of homeostasis is potentially one of the most studied and understood aspects of physiology. Also well known are the effects of threats to homeostasis, known as stressors. It has long been appreciated that the body responds to stressors actively, known as an allostatic response. The classic stress response – the activation of the sympathetic nervous system and the release of glucocorticoids from the adrenal glands – has been well studied, though perhaps it has been painted in a somewhat negative light as being detrimental to health. In fact, stress responses are necessary for the survival of an organism when it faces a threat to homeostasis, and so in the acute sense, stress is beneficial. The cost of restoring normal homeostasis through active intervention is known as allostatic load. This load, be it through chronic stress, or malfunctions in the systems regulating allostasis, can lead to wear and tear on the brain and body, with significant implications for mental and physical health. This chapter will summarize how stress, and the allostatic responses that accompany stress, affects physical and psychological health. We will discuss how chronic stress and allostatic overload can contribute to disease states and affect disease progression and the role of the body΄s circadian (daily) timing systems: what they mean for maintaining homeostasis and how disruption of circadian timing may lead to allostatic load and overload. [ABSTRACT FROM AUTHOR]

Published
2010
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11. Allosteric Potentiators of Neuronal Nicotinic Cholinergic Receptors: Potential Treatments for Neurodegenerative Disorders.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Sher, Emanuele, Filippi, Giovanna De, Baldwinson, Tristan, Zwart, Ruud, Pearson, Kathy H., Lee, Martin, Wallace, Louise, McPhie, Gordon I., Keenan, Martine, and Emkey, Renee

Published
2008
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12. Dissociation Between the Potent β-Amyloid Protein Pathway Inhibition and Cholinergic Actions of the Alzheimer Drug Candidates Phenserine and Cymserine.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Greig, Nigel H., Utsuki, Tada, Yu, Qian-sheng, Holloway, Harold W., Perry, Tracyann, Tweedie, David, Giordano, Tony, Alley, George M., Chen, De-Mao, and Kamal, Mohammad A.

Published
2008
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21. Up-regulation of the α-Secretase Pathway.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Fahrenholz, Falk, Prinzen, Claudia, Postina, Rolf, and Kojro, Elżbieta

Published
2008
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25. Cell Models of Tauopathy.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Biernat, J., Khlistunova, I., Wang, Y-P., Pickhardt, M., Bergen, M. von, Gazova, Z., Mandelkow, Eckhart, and Mandelkow, Eva-Marie

Published
2008
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29. Intraneuronal Aβ and Alzheimer's Disease.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Billings, Lauren M., and LaFerla, Frank M.

Published
2008
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35. Stem Cell Therapy in Alzheimer's Disease.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Sugaya, Kiminobu, Kwak, Young-Don, and Alvarez, Angel

Published
2008
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41. Alzheimer's Disease Neuroimaging Initiative.

Author

Bures, Jan, Kopin, Irwin, McEwen, Bruce, Pribram, Karl, Rosenblatt, Jay, Weiskranz, Lawrence, Fisher, Abraham, Memo, Maurizio, Stocchi, Fabrizio, Hanin, Israel, Mueller, Susanne G., Weiner, Michael W., Thal, Leon J., Petersen, Ronald C., Jack, Clifford, Jagust, William, Trojanowski, John Q., Toga, Arthur W, and Beckett, Laurel

Published
2008
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