Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity - Wikidata - wikimedia - TriplyDB

Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity

Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity

http://www.wikidata.org/entity/Q35973444

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Sculpting the hippocampus from within: stress, spines, and CRH Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle Are Anxiety Disorders Associated with Accelerated Aging? A Focus on Neuroprogression Sleep, circadian rhythms, and the pathogenesis of Alzheimer disease Exploring the relationship between personality and regional brain volume in healthy aging Posttraumatic stress disorder-like induction elevates β-amyloid levels, which directly activates corticotropin-releasing factor neurons to exacerbate stress responses.The effects of meditation on perceived stress and related indices of psychological status and sympathetic activation in persons with Alzheimer's disease and their caregivers: a pilot study.Central CRF system perturbation in an Alzheimer's disease knockin mouse model.Corticotropin-releasing factor receptor-1 antagonism mitigates beta amyloid pathology and cognitive and synaptic deficits in a mouse model of Alzheimer's disease.Relationship between plasma analytes and SPARE-AD defined brain atrophy patterns in ADNI Mechanism of neuronal versus endothelial cell uptake of Alzheimer's disease amyloid beta protein Corticotropin-releasing factor overexpression gives rise to sex differences in Alzheimer's disease-related signaling.3xTgAD mice exhibit altered behavior and elevated Aβ after chronic mild social stress Targeting psychologic stress signaling pathways in Alzheimer's disease.Pathways linking late-life depression to persistent cognitive impairment and dementia.Lack of Social Support Raises Stress Vulnerability in Rats with a History of Ancestral Stress.Effects of stress and stress hormones on amyloid-beta protein and plaque deposition.Stress-induced tau phosphorylation: functional neuroplasticity or neuronal vulnerability?Gene-environment interaction research and transgenic mouse models of Alzheimer's disease.Traumatic brain injury reduces soluble extracellular amyloid-β in mice: a methodologically novel combined microdialysis-controlled cortical impact study.Effects of age and amyloid deposition on Aβ dynamics in the human central nervous system.Brain neurotoxic amyloid-beta peptides: their potential role in the pathophysiology of depression and as molecular therapeutic targets.Effects of corticotrophin-releasing factor receptor 1 antagonists on amyloid-β and behavior in Tg2576 mice.Absence of ALOX5 gene prevents stress-induced memory deficits, synaptic dysfunction and tauopathy in a mouse model of Alzheimer's disease.Lipopolysaccharide-induced tau phosphorylation and kinase activity--modulation, but not mediation, by corticotropin-releasing factor receptors.Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?Amyloid-β efflux from the central nervous system into the plasma.Effects of growth hormone-releasing hormone on sleep and brain interstitial fluid amyloid-β in an APP transgenic mouse model The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer's disease.Chronic stress exacerbates tau pathology, neurodegeneration, and cognitive performance through a corticotropin-releasing factor receptor-dependent mechanism in a transgenic mouse model of tauopathy A lifespan view of anxiety disorders.Impact of CRFR1 Ablation on Amyloid-β Production and Accumulation in a Mouse Model of Alzheimer's Disease.The stress response neuropeptide CRF increases amyloid-β production by regulating γ-secretase activity Corticotropin-releasing factor receptor-dependent effects of repeated stress on tau phosphorylation, solubility, and aggregation.Chronic Noise Exposure Acts Cumulatively to Exacerbate Alzheimer's Disease-Like Amyloid-β Pathology and Neuroinflammation in the Rat Hippocampus Restraint stress and repeated corticotrophin-releasing factor receptor activation in the amygdala both increase amyloid-β precursor protein and amyloid-β peptide but have divergent effects on brain-derived neurotrophic factor and pre-synaptic protei Locus Coeruleus, norepinephrine and Aβ peptides in Alzheimer's disease Corticotrophin releasing factor accelerates neuropathology and cognitive decline in a mouse model of Alzheimer's disease.Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo Short-term modern life-like stress exacerbates Aβ-pathology and synapse loss in 3xTg-AD mice

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Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity

http://www.wikidata.org/entity/Q35973444

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2007 nî lūn-bûn

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Acute stress increases interst ...... g factor and neuronal activity

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Proceedings of the National Academy of Sciences of the United States of America

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Acute stress increases interst ...... g factor and neuronal activity

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Hongxin Dong

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Jae-Eun Kang

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John G Csernansky

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John R Cirrito

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P2860

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Influence of education and occupation on the incidence of Alzheimer's disease

Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective

Molecular, structural, and functional characterization of Alzheimer's disease: evidence for a relationship between default activity, amyloid, and memory

APP processing and synaptic function

Characterization of a 41-residue ovine hypothalamic peptide that stimulates secretion of corticotropin and beta-endorphin

Environmental enrichment mitigates cognitive deficits in a mouse model of Alzheimer's disease

Brain work and brain imaging.

Hippocampal corticotropin releasing hormone: pre- and postsynaptic location and release by stress.

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent.

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10673-10678

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104

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David M. Holtzman

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