Cerebral amyloid angiopathy, blood-brain barrier disruption and amyloid accumulation in SAMP8 mice

Jaume Del Valle, Joaquim Duran-Vilaregut, Gemma Manich, Mercè Pallàs, Antoni Camins, Jordi Vilaplana, Carme Pelegrí*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

33 Citations (Scopus)

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.

Original languageAmerican English
Pages (from-to)421-429
Number of pages9
JournalNeurodegenerative Diseases
Volume8
Issue number6
DOIs
Publication statusPublished - Jul 2011

Keywords

  • Alzheimer's disease
  • Amyloid accumulation
  • Blood-brain barrier
  • Cerebral amyloid angiopathy
  • Late-onset Alzheimer's disease
  • SAMP8 mice

Fingerprint

Dive into the research topics of 'Cerebral amyloid angiopathy, blood-brain barrier disruption and amyloid accumulation in SAMP8 mice'. Together they form a unique fingerprint.

Cite this