Brain and Circulating Levels of A β 1–40 Differentially Contribute to Vasomotor Dysfunction in the Mouse Brain
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C. Iadecola | M. L. Previti | W. V. Nostrand | K. Koizumi | Sleiman El Jamal | Ping Zhou | Laibaik Park | Ping Zhou | George Carlson
[1] L. Mucke,et al. Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. , 2012, Cold Spring Harbor perspectives in medicine.
[2] S. Rivest,et al. The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease , 2012, The European journal of neuroscience.
[3] S. Greenberg,et al. The Pathophysiology and Clinical Presentation of Cerebral Amyloid Angiopathy , 2012, Current Atherosclerosis Reports.
[4] C. Iadecola,et al. Central Cardiovascular Circuits Contribute to the Neurovascular Dysfunction in Angiotensin II Hypertension , 2012, The Journal of Neuroscience.
[5] Mark A. van Buchem,et al. Monitoring blood flow alterations in the Tg2576 mouse model of Alzheimer's disease by in vivo magnetic resonance angiography at 17.6T , 2012, NeuroImage.
[6] B. Zlokovic. Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders , 2011, Nature Reviews Neuroscience.
[7] D. Bennett,et al. Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association , 2011, Stroke.
[8] P. Carmeliet,et al. The Neurovascular Link in Health and Disease: Molecular Mechanisms and Therapeutic Implications , 2011, Neuron.
[9] Clifford R. Jack,et al. Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: Recommendations from the Alzheimer’s Association Research Roundtable Workgroup , 2011, Alzheimer's & Dementia.
[10] C. Iadecola,et al. Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-β , 2011, Proceedings of the National Academy of Sciences.
[11] C. Iadecola. The overlap between neurodegenerative and vascular factors in the pathogenesis of dementia , 2010, Acta Neuropathologica.
[12] E. Siemers,et al. Safety and Changes in Plasma and Cerebrospinal Fluid Amyloid &bgr; After a Single Administration of an Amyloid &bgr; Monoclonal Antibody in Subjects With Alzheimer Disease , 2010, Clinical neuropharmacology.
[13] T. Ogihara,et al. Angiotensin Receptor Blocker Prevented &bgr;-Amyloid–Induced Cognitive Impairment Associated With Recovery of Neurovascular Coupling , 2009, Hypertension.
[14] T. Sobrino,et al. Plasma &bgr;-Amyloid 1-40 Is Associated With the Diffuse Small Vessel Disease Subtype , 2009, Stroke.
[15] R. Silverstein,et al. CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior , 2009, Science Signaling.
[16] C. Iadecola,et al. Threats to the Mind: Aging, Amyloid, and Hypertension , 2009, Stroke.
[17] R. Weller,et al. Microvasculature changes and cerebral amyloid angiopathy in Alzheimer’s disease and their potential impact on therapy , 2009, Acta Neuropathologica.
[18] C. Adler,et al. Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer's disease , 2009, Alzheimer's & Dementia.
[19] David M Holtzman,et al. Cerebrovascular Dysfunction in Amyloid Precursor Protein Transgenic Mice: Contribution of Soluble and Insoluble Amyloid-β Peptide, Partial Restoration via γ-Secretase Inhibition , 2008, The Journal of Neuroscience.
[20] B. Zlokovic. The Blood-Brain Barrier in Health and Chronic Neurodegenerative Disorders , 2008, Neuron.
[21] M. D'Andrea,et al. Aβ peptides can enter the brain through a defective blood–brain barrier and bind selectively to neurons , 2007, Brain Research.
[22] A. Hofman,et al. Cerebral hypoperfusion and clinical onset of dementia: The Rotterdam study , 2005, Annals of neurology.
[23] R. Deane,et al. Early-onset and Robust Cerebral Microvascular Accumulation of Amyloid β-Protein in Transgenic Mice Expressing Low Levels of a Vasculotropic Dutch/Iowa Mutant Form of Amyloid β-Protein Precursor* , 2004, Journal of Biological Chemistry.
[24] D. Holtzman,et al. Apolipoprotein E Markedly Facilitates Age-Dependent Cerebral Amyloid Angiopathy and Spontaneous Hemorrhage in Amyloid Precursor Protein Transgenic Mice , 2003, The Journal of Neuroscience.
[25] C. Iadecola,et al. Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein. , 2002, American journal of physiology. Heart and circulatory physiology.
[26] George A. Carlson,et al. Exogenous Aβ1–40 Reproduces Cerebrovascular Alterations Resulting from Amyloid Precursor Protein Overexpression in Mice , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[27] C. Iadecola,et al. Abeta 1-40-related reduction in functional hyperemia in mouse neocortex during somatosensory activation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[28] D. Borchelt,et al. SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein , 1999, Nature Neuroscience.
[29] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[30] C. Iadecola,et al. Nitric oxide participates in the cerebrovasodilation elicited from cerebellar fastigial nucleus. , 1992, The American journal of physiology.
[31] F. Schmitt,et al. Plasma amyloid-β as a function of age, level of intellectual disability, and presence of dementia in Down syndrome. , 2011, Journal of Alzheimer's disease : JAD.
[32] A. Hofman,et al. Plasma Abeta(1-40) and Abeta(1-42) and the risk of dementia: a prospective case-cohort study. , 2006, The Lancet. Neurology.
[33] T. Golde,et al. Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse model. , 2006, The Journal of clinical investigation.
[34] J. Growdon,et al. Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy. , 2006, Neurology.
[35] C. Iadecola,et al. NADPH-oxidase-derived reactive oxygen species mediate the cerebrovascular dysfunction induced by the amyloid beta peptide. , 2005, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[36] L S Honig,et al. Plasma A[beta]40 and A[beta]42 and Alzheimer's disease: relation to age, mortality, and risk. , 2003, Neurology.
[37] F. Crawford,et al. Vasoactive effects of A beta in isolated human cerebrovessels and in a transgenic mouse model of Alzheimer's disease: role of inflammation. , 2003, Neurological research.
[38] J. Berman,et al. CD36, a class B scavenger receptor, is expressed on microglia in Alzheimer's disease brains and can mediate production of reactive oxygen species in response to beta-amyloid fibrils. , 2002, The American journal of pathology.
[39] D. Holtzman,et al. Peripheral anti-A beta antibody alters CNS and plasma A beta clearance and decreases brain A beta burden in a mouse model of Alzheimer's disease. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[40] S. Younkin,et al. Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease. , 2001, The Journal of neuroscience : the official journal of the Society for Neuroscience.