Brain and Circulating Levels of A β 1–40 Differentially Contribute to Vasomotor Dysfunction in the Mouse Brain

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[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.