Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein. - Test2 - elhamkhani - TriplyDB

Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

http://www.wikidata.org/entity/Q30481236

about

Threats to the mind: aging, amyloid, and hypertension Cerebral Small Vessel Disease: Targeting Oxidative Stress as a Novel Therapeutic Strategy?Vascular contributions to cognitive impairment and dementia including Alzheimer's disease Evolution of NADPH Oxidase Inhibitors: Selectivity and Mechanisms for Target Engagement Redox control of microglial function: molecular mechanisms and functional significance The pathobiology of vascular dementia Oxidized cholesterol as the driving force behind the development of Alzheimer's disease Hypertension: a harbinger of stroke and dementia Aging-related alterations in eNOS and nNOS responsiveness and smooth muscle reactivity of murine basilar arteries are modulated by apocynin and phosphorylation of myosin phosphatase targeting subunit-1 Oxidation-Responsive, EuII/III-Based, Multimodal Contrast Agent for Magnetic Resonance and Photoacoustic Imaging Limitations of collateral flow after occlusion of a single cortical penetrating arteriole Triterpenoid CDDO-methylamide improves memory and decreases amyloid plaques in a transgenic mouse model of Alzheimer's disease.Water deprivation induces neurovascular and cognitive dysfunction through vasopressin-induced oxidative stress Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice.Cyclooxygenase 1-derived prostaglandin E2 and EP1 receptors are required for the cerebrovascular dysfunction induced by angiotensin II.A palette of fluorescent probes with varying emission colors for imaging hydrogen peroxide signaling in living cells Estrogen attenuates ischemic oxidative damage via an estrogen receptor alpha-mediated inhibition of NADPH oxidase activation The cerebrovascular dysfunction induced by slow pressor doses of angiotensin II precedes the development of hypertension European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).NOX activity is increased in mild cognitive impairment Transgenic mice overexpressing amyloid precursor protein exhibit early metabolic deficits and a pathologically low leptin state associated with hypothalamic dysfunction in arcuate neuropeptide Y neurons Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association.Role of vascular risk factors and vascular dysfunction in Alzheimer's disease.Vascular and metabolic dysfunction in Alzheimer's disease: a review.Targeting NOX enzymes in the central nervous system: therapeutic opportunities.Endothelin 1-dependent neurovascular dysfunction in chronic intermittent hypoxia.Ibuprofen attenuates oxidative damage through NOX2 inhibition in Alzheimer's disease Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease The overlap between neurodegenerative and vascular factors in the pathogenesis of dementia Proliferative neural stem cells have high endogenous ROS levels that regulate self-renewal and neurogenesis in a PI3K/Akt-dependant manner.Brain and circulating levels of Aβ1-40 differentially contribute to vasomotor dysfunction in the mouse brain.Nox2 redox signaling maintains essential cell populations in the brain.Oxidative stress, redox signalling and endothelial dysfunction in ageing-related neurodegenerative diseases: a role of NADPH oxidase 2.Genome-wide alteration of histone H3K9 acetylation pattern in mouse offspring prenatally exposed to arsenic Resveratrol treatment rescues neurovascular coupling in aged mice: role of improved cerebromicrovascular endothelial function and downregulation of NADPH oxidase.The role of the NADPH oxidase NOX2 in prion pathogenesis.Cognitive and cerebrovascular improvements following kinin B1 receptor blockade in Alzheimer's disease mice.Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice.Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-beta.Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation.

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P2860

Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

http://www.wikidata.org/entity/Q30481236

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Nox2-derived radicals contribu ...... the amyloid precursor protein.

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Nox2-derived radicals contribu ...... the amyloid precursor protein.

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Nox2-derived radicals contribu ...... the amyloid precursor protein.

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P2860

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

Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype.

The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

Mouse model of X-linked chronic granulomatous disease, an inherited defect in phagocyte superoxide production

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

Neurovascular regulation in the normal brain and in Alzheimer's disease

Cyclooxygenase-1 participates in selected vasodilator responses of the cerebral circulation.

A beta-peptides enhance vasoconstriction in cerebral circulation.

NADPH-oxidase-derived reactive oxygen species mediate the cerebrovascular dysfunction induced by the amyloid beta peptide.

Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease.

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