We are analyzing https://link.springer.com/article/10.1007/s00401-011-0801-7.

Title:
Perivascular drainage of solutes is impaired in the ageing mouse brain and in the presence of cerebral amyloid angiopathy | Acta Neuropathologica
Description:
The deposition of amyloid-β (Aβ) peptides in the walls of leptomeningeal and cortical blood vessels as cerebral amyloid angiopathy (CAA) is present in normal ageing and the majority of Alzheimer’s disease (AD) brains. The failure of clearance mechanisms to eliminate Aβ from the brain contributes to the development of sporadic CAA and AD. Here, we investigated the effects of CAA and ageing on the pattern of perivascular drainage of solutes in the brains of naïve mice and in the Tg2576 mouse model of AD. We report that drainage of small molecular weight dextran along cerebrovascular basement membranes is impaired in the hippocampal capillaries and arteries of 22-month-old wild-type mice compared to 3- and 7-month-old animals, which was associated with age-dependent changes in capillary density. Age-related alterations in the levels of laminin, fibronectin and perlecan in vascular basement membranes were also noted in wild-type mice. Furthermore, dextran was observed in the walls of veins of Tg2576 mice in the presence of CAA, suggesting that deposition of Aβ in vessel walls disrupts the normal route of elimination of solutes from the brain parenchyma. These data support the hypothesis that perivascular solute drainage from the brain is altered both in the ageing brain and as a consequence of CAA. These findings have implications for the success of therapeutic strategies for the treatment of AD that rely upon the health of the ageing cerebral vasculature.
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Keywords {🔍}

pubmed, google, scholar, article, cas, amyloid, cerebral, alzheimers, disease, brain, angiopathy, mice, perivascular, basement, mouse, transgenic, van, drainage, neuropathol, neurosci, neurobiol, aging, ageing, cerebrovascular, weller, membranes, beta, acta, deposition, model, vascular, protein, pathol, solutes, nicoll, blood, caa, access, peptide, privacy, cookies, content, research, carare, perlecan, alzheimer, human, sci, fibril, cell,

Topics {✒️}

month download article/chapter amyloid beta-protein fibril aged app/ps1 mice inducing cd4+cd25− lap + transforming growth factor-beta1 insoluble amyloid-beta peptide amyloid-beta peptide remnants wild-type mice compared amyloid precursor protein beta-amyloid protein amyloid beta-protein blood–brain barrier disorder ageing cerebral vasculature full article pdf increased vascular amyloid app-transgenic mice age-dependent cerebrovascular dysfunction cerebral amyloid angiopathy passive anti-aβ immunotherapy amyloid-β vascular basement membranes amyloid beta peptide transgenic mouse model privacy choices/manage cookies transgenic mice overexpressing wild-type mice cerebrovascular basement membranes beta-amyloid proteins cns beta-amyloid mice lacking heparin amyloid beta deposition axonal transport deficits perivascular solute drainage perivascular drainage channels tg2576 mouse model human cerebral microvessels research trust uk transgenic mouse models basement membrane components cerebral microvascular alterations mammalian basement membranes amyloid beta peptides amyloid-beta peptides basement membrane proteoglycans reverse perivascular transport amyloid plaque-related van den haute cerebrovascular dysfunction induced hereditary cerebral hemorrhage heparan sulfate proteoglycans

Questions {❓}

Is CAA a perivascular brain clearance disease?
Knox SM, Whitelock JM (2006) Perlecan: how does one molecule do so many things?

Schema {🗺️}

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         description:The deposition of amyloid-β (Aβ) peptides in the walls of leptomeningeal and cortical blood vessels as cerebral amyloid angiopathy (CAA) is present in normal ageing and the majority of Alzheimer’s disease (AD) brains. The failure of clearance mechanisms to eliminate Aβ from the brain contributes to the development of sporadic CAA and AD. Here, we investigated the effects of CAA and ageing on the pattern of perivascular drainage of solutes in the brains of naïve mice and in the Tg2576 mouse model of AD. We report that drainage of small molecular weight dextran along cerebrovascular basement membranes is impaired in the hippocampal capillaries and arteries of 22-month-old wild-type mice compared to 3- and 7-month-old animals, which was associated with age-dependent changes in capillary density. Age-related alterations in the levels of laminin, fibronectin and perlecan in vascular basement membranes were also noted in wild-type mice. Furthermore, dextran was observed in the walls of veins of Tg2576 mice in the presence of CAA, suggesting that deposition of Aβ in vessel walls disrupts the normal route of elimination of solutes from the brain parenchyma. These data support the hypothesis that perivascular solute drainage from the brain is altered both in the ageing brain and as a consequence of CAA. These findings have implications for the success of therapeutic strategies for the treatment of AD that rely upon the health of the ageing cerebral vasculature.
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