title: Cerebral amyloid angiopathy, blood-brain barrier disruption and amyloid accumulation in SAMP8 mice.
abstract: Cerebrovascular dysfunction and β-amyloid peptide deposition on the walls of cerebral blood vessels might be an early event in the development of Alzheimer's disease. Here we studied the time course of amyloid deposition in blood vessels and blood-brain barrier (BBB) disruption in the CA1 subzone of the hippocampus of SAMP8 mice and the association between these two variables. We also studied the association between the amyloid deposition in blood vessels and the recently described amyloid clusters in the parenchyma, as well as the association of these clusters with vessels in which the BBB is disrupted. SAMP8 mice showed greater amyloid deposition in blood vessels than age-matched ICR-CD1 control mice. Moreover, at 12 months of age the number of vessels with a disrupted BBB had increased in both strains, especially SAMP8 animals. At this age, all the vessels with amyloid deposition showed BBB disruption, but several capillaries with an altered BBB showed no amyloid on their walls. Moreover, amyloid clusters showed no spatial association with vessels with amyloid deposition, nor with vessels in which the BBB had been disrupted. Finally, we can conclude that vascular amyloid deposition seems to induce BBB alterations, but BBB disruption may also be due to other factors.
authors.affiliation: Departament de Fisiologia, Facultat de Farmàcia, Barcelona, Spain.
authors.forename: Jaume
authors.initials: J
authors.lastname: del Valle
authors.forename: Joaquim
authors.initials: J
authors.lastname: Duran-Vilaregut
authors.forename: Gemma
authors.initials: G
authors.lastname: Manich
authors.forename: Mercè
authors.initials: M
authors.lastname: Pallàs
authors.forename: Antoni
authors.initials: A
authors.lastname: Camins
authors.forename: Jordi
authors.initials: J
authors.lastname: Vilaplana
authors.forename: Carme
authors.initials: C
authors.lastname: Pelegrí
mesh_terms: D000375:Aging / Q000502:physiology; D000682:Amyloid / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001808:Blood Vessels / Q000187:drug effects / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000473:pathology*; D016657:Cerebral Amyloid Angiopathy / Q000235:genetics* / Q000473:pathology; D006624:Hippocampus / Q000098:blood supply / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008822:Mice, Transgenic; D008856:Microscopy, Fluorescence; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D012039:Regional Blood Flow / Q000502:physiology
chemical_list: D000682:Amyloid; D016229:Amyloid beta-Peptides; D007074:Immunoglobulin G; D019408:Platelet Endothelial Cell Adhesion Molecule-1