FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2223248886> ?p ?o ?g. }

• W2223248886 endingPage "117" @default.
• W2223248886 startingPage "107" @default.
• W2223248886 abstract "Clinical and experimental evidence point to a possible role of cerebrovascular dysfunction in Alzheimer's disease (AD). The 5xFAD mouse model of AD expresses human amyloid precursor protein and presenilin genes with mutations found in AD patients. It remains unknown whether amyloid deposition driven by these mutations is associated with cerebrovascular changes. 5xFAD and wild type mice (2 to 12 months old; M2 to M12) were used. Thinned skull in vivo 2-photon microscopy was used to determine Aβ accumulation on leptomeningeal or superficial cortical vessels over time. Parenchymal microvascular damage was assessed using FITC-microangiography. Collagen-IV and CD31 were used to stain basal lamina and endothelial cells. Methoxy-XO4, Thioflavin-S or 6E10 were used to visualize Aβ accumulation in living mice or in fixed brain tissues. Positioning of reactive IBA1 microglia and GFAP astrocytes at the vasculature was rendered using confocal microscopy. Platelet-derived growth factor receptor beta (PDGFRβ) staining was used to visualize perivascular pericytes. In vivo 2-photon microscopy revealed Methoxy-XO4+ amyloid perivascular deposits on leptomeningeal and penetrating cortical vessels in 5xFAD mice, typical of cerebral amyloid angiopathy (CAA). Amyloid deposits were visible in vivo at M3 and aggravated over time. Progressive microvascular damage was concomitant to parenchymal Aβ plaque accumulation in 5xFAD mice. Microvascular inflammation in 5xFAD mice presented with sporadic FITC-albumin leakages at M4 becoming more prevalent at M9 and M12. 3D colocalization showed inflammatory IBA1+ microglia proximal to microvascular FITC-albumin leaks. The number of perivascular PDGFRβ+ pericytes was significantly decreased at M4 in the fronto-parietal cortices, with a trend decrease observed in the other structures. At M9–M12, PDGFRβ+ pericytes displayed hypertrophic perivascular ramifications contiguous to reactive microglia. Cerebral amyloid angiopathy and microvascular inflammation occur in 5xFAD mice concomitantly to parenchymal plaque deposition. The prospect of cerebrovascular pharmacology in AD is discussed." @default.
• W2223248886 created "2016-06-24" @default.
• W2223248886 creator A5001578819 @default.
• W2223248886 creator A5019411902 @default.
• W2223248886 creator A5026648305 @default.
• W2223248886 creator A5027491160 @default.
• W2223248886 creator A5040826567 @default.
• W2223248886 creator A5062158733 @default.
• W2223248886 creator A5065180611 @default.
• W2223248886 creator A5072148725 @default.
• W2223248886 creator A5082955260 @default.
• W2223248886 date "2016-04-01" @default.
• W2223248886 modified "2023-10-13" @default.
• W2223248886 title "Cerebrovascular pathology during the progression of experimental Alzheimer's disease" @default.
• W2223248886 cites W1531467877 @default.
• W2223248886 cites W1729585270 @default.
• W2223248886 cites W1815758482 @default.
• W2223248886 cites W1824128114 @default.
• W2223248886 cites W1841850981 @default.
• W2223248886 cites W1957213374 @default.
• W2223248886 cites W1977585036 @default.
• W2223248886 cites W1979218016 @default.
• W2223248886 cites W1979221664 @default.
• W2223248886 cites W1985063020 @default.
• W2223248886 cites W1985402737 @default.
• W2223248886 cites W1989718007 @default.
• W2223248886 cites W2003762128 @default.
• W2223248886 cites W2009869050 @default.
• W2223248886 cites W2015541518 @default.
• W2223248886 cites W2018149927 @default.
• W2223248886 cites W2019780808 @default.
• W2223248886 cites W2025774809 @default.
• W2223248886 cites W2028372123 @default.
• W2223248886 cites W2029609315 @default.
• W2223248886 cites W2034275438 @default.
• W2223248886 cites W2040571516 @default.
• W2223248886 cites W2043407651 @default.
• W2223248886 cites W2054162453 @default.
• W2223248886 cites W2056856515 @default.
• W2223248886 cites W2061441842 @default.
• W2223248886 cites W2073290778 @default.
• W2223248886 cites W2073370423 @default.
• W2223248886 cites W2074546602 @default.
• W2223248886 cites W2083254102 @default.
• W2223248886 cites W2084970815 @default.
• W2223248886 cites W2098613848 @default.
• W2223248886 cites W2098977708 @default.
• W2223248886 cites W2100007022 @default.
• W2223248886 cites W2102493638 @default.
• W2223248886 cites W2104701727 @default.
• W2223248886 cites W2106914633 @default.
• W2223248886 cites W2107431414 @default.
• W2223248886 cites W2109290881 @default.
• W2223248886 cites W2111570868 @default.
• W2223248886 cites W2126019582 @default.
• W2223248886 cites W2133395047 @default.
• W2223248886 cites W2142740085 @default.
• W2223248886 cites W2143238511 @default.
• W2223248886 cites W2150972825 @default.
• W2223248886 cites W2152719134 @default.
• W2223248886 cites W2154656101 @default.
• W2223248886 cites W2155941173 @default.
• W2223248886 cites W2156965724 @default.
• W2223248886 cites W2158547909 @default.
• W2223248886 cites W2158762199 @default.
• W2223248886 cites W2159821105 @default.
• W2223248886 cites W2165503155 @default.
• W2223248886 cites W2167183660 @default.
• W2223248886 cites W2170644095 @default.
• W2223248886 cites W274427711 @default.
• W2223248886 cites W654966828 @default.
• W2223248886 doi "https://doi.org/10.1016/j.nbd.2016.01.001" @default.
• W2223248886 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26774030" @default.
• W2223248886 hasPublicationYear "2016" @default.
• W2223248886 type Work @default.
• W2223248886 sameAs 2223248886 @default.
• W2223248886 citedByCount "98" @default.
• W2223248886 countsByYear W22232488862016 @default.
• W2223248886 countsByYear W22232488862017 @default.
• W2223248886 countsByYear W22232488862018 @default.
• W2223248886 countsByYear W22232488862019 @default.
• W2223248886 countsByYear W22232488862020 @default.
• W2223248886 countsByYear W22232488862021 @default.
• W2223248886 countsByYear W22232488862022 @default.
• W2223248886 countsByYear W22232488862023 @default.
• W2223248886 crossrefType "journal-article" @default.
• W2223248886 hasAuthorship W2223248886A5001578819 @default.
• W2223248886 hasAuthorship W2223248886A5019411902 @default.
• W2223248886 hasAuthorship W2223248886A5026648305 @default.
• W2223248886 hasAuthorship W2223248886A5027491160 @default.
• W2223248886 hasAuthorship W2223248886A5040826567 @default.
• W2223248886 hasAuthorship W2223248886A5062158733 @default.
• W2223248886 hasAuthorship W2223248886A5065180611 @default.
• W2223248886 hasAuthorship W2223248886A5072148725 @default.
• W2223248886 hasAuthorship W2223248886A5082955260 @default.
• W2223248886 hasBestOaLocation W22232488862 @default.
• W2223248886 hasConcept C123012128 @default.
• W2223248886 hasConcept C142724271 @default.

• next