Abstract | INTRODUCTION: METHODS: RESULTS: While total β- amyloid (Aβ) load is unchanged across groups, Congophilic amyloid deposition was decreased in the parenchyma and significantly increased in the vasculature as cerebral amyloid angiopathy (CAA; vascular amyloid deposition) in HHcy APP/PS1 mice. We also found that HHcy induced more microhemorrhages in the APP/PS1 mice than in the wild-type mice and that it switched the neuroinflammatory phenotype from an M2a biased state to an M1 biased state. Associated with these changes was an induction of the matrix metalloproteinase protein 2 (MMP2) and MMP9 systems. Interestingly, after 6 months of HHcy, the APP/PS1 mice were cognitively worse than wild-type HHcy mice or APP/PS1 mice, indicative of an additive effect of the cerebrovascular pathology and amyloid deposition. CONCLUSIONS:
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Authors | Tiffany L Sudduth, Erica M Weekman, Holly M Brothers, Kaitlyn Braun, Donna M Wilcock |
Journal | Alzheimer's research & therapy
(Alzheimers Res Ther)
Vol. 6
Issue 3
Pg. 32
( 2014)
ISSN: 1758-9193 [Print] England |
PMID | 24991237
(Publication Type: Journal Article)
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