Serum Amyloid P Immunoreactivity in Cortical Tangles, Plaques and Vessels in Alzheimer’s Disease: Implications for Dysfunction of the Blood-Brain Barrier?

[1]  R. Kalaria,et al.  Increased α 2- and β 2-adrenergic receptors in cerebral microvessels in Alzheimer disease , 1989, Neuroscience Letters.

[2]  R N Kalaria,et al.  Reduced Glucose Transporter at the Blood‐Brain Barrier and in Cerebral Cortex in Alzheimer Disease , 1989, Journal of neurochemistry.

[3]  W. Kamphorst,et al.  Lack of evidence for dysfunction of the blood-brain barrier in Alzhiemer's disease: An immunohistochemical study , 1988, Neurobiology of Aging.

[4]  S. V. van Duinen,et al.  Isolation and characterization of amyloid P component from Alzheimer's disease and other types of cerebral amyloidosis. , 1988, Laboratory investigation; a journal of technical methods and pathology.

[5]  J. Hardy,et al.  An integrative hypothesis concerning the pathogenesis and progression of Alzheimer's disease , 1986, Neurobiology of Aging.

[6]  K. Shimada,et al.  Isolation and characterization of the complete complementary and genomic DNA sequences of human serum amyloid P component. , 1986, Journal of biochemistry.

[7]  P. D. Lewis,et al.  IMMUNOHISTOCHEMICAL DEMONSTRATION OF AMYLOID P COMPONENT IN CEREBRO‐VASCULAR AMYLOIDOSIS , 1984, Neuropathology and applied neurobiology.

[8]  A. Brun,et al.  Immunohistochemical evidence for the lack of amyloid P component in some intracerebral amyloids. , 1982, Laboratory investigation; a journal of technical methods and pathology.

[9]  G. Glenner Amyloid deposits and amyloidosis. The beta-fibrilloses (first of two parts). , 1980, The New England journal of medicine.