Disassembly of amyloid β-protein fibril by basement membrane components

Kiuchi, Yoichi; Isobe, Yoshihiko; Fukushima, Kiyomi; Kimura, Masaaki

doi:10.1016/s0024-3205(02)01501-1

Cited by 23 publications

(14 citation statements)

References 29 publications

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“…Laminin, nidogens, and collagen IV inhibit the aggregation of Aβ and destabilize pre-formed fibrils of Aβ in vitro , while HSPG agrin and perlecan accelerate its aggregation (Aumailley and Krieg, 1996; Bronfman et al, 1996, 1998; Castillo et al, 1997; Cotman et al, 2000; Kiuchi et al, 2002a,b). Decreased amounts of collagen IV have been reported in small diameter vessels (<50 μm) from AD patients compared to aged-matched controls (Christov et al, 2008).…”

Section: Role Of Cvbm and Perivascular Drainage In Caamentioning

confidence: 99%

The Cerebrovascular Basement Membrane: Role in the Clearance of Î²-amyloid and Cerebral Amyloid Angiopathy

Morris

Carare

Schreiber

et al. 2014

Front. Aging Neurosci.

103

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Cerebral amyloid angiopathy (CAA), the accumulation of β-amyloid (Aβ) peptides in the walls of cerebral blood vessels, is observed in the majority of Alzheimer’s disease (AD) brains and is thought to be due to a failure of the aging brain to clear Aβ. Perivascular drainage of Aβ along cerebrovascular basement membranes (CVBMs) is one of the mechanisms by which Aβ is removed from the brain. CVBMs are specialized sheets of extracellular matrix that provide structural and functional support for cerebral blood vessels. Changes in CVBM composition and structure are observed in the aged and AD brain and may contribute to the development and progression of CAA. This review summarizes the properties of the CVBM, its role in mediating clearance of interstitial fluids and solutes from the brain, and evidence supporting a role for CVBM in the etiology of CAA.

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Section: Role Of Cvbm and Perivascular Drainage In Caamentioning

confidence: 99%

The Cerebrovascular Basement Membrane: Role in the Clearance of Î²-amyloid and Cerebral Amyloid Angiopathy

Morris

Carare

Schreiber

et al. 2014

Front. Aging Neurosci.

103

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“…Several lines of evidence suggest that biochemical and morphological alterations to basement membranes contribute to the development of CAA. In vitro incubation of Ab with laminin, collagen IV, and nidogen has been shown to prevent Ab fibrillization, whereas agrin and perlecan promote and stabilize Ab fiber formation (Castillo et al, 1997;Bronfman et al, 1998;Cotman et al, 2000;Kiuchi et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Regional differences in the morphological and functional effects of aging on cerebral basement membranes and perivascular drainage of amyloid‐β from the mouse brain

et al. 2013

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SummaryDevelopment of cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD) is associated with failure of elimination of amyloid-b (Ab) from the brain along perivascular basement membranes that form the pathways for drainage of interstitial fluid and solutes from the brain. In transgenic APP mouse models of AD, the severity of cerebral amyloid angiopathy is greater in the cerebral cortex and hippocampus, intermediate in the thalamus, and least in the striatum. In this study we test the hypothesis that age-related regional variation in (1) vascular basement membranes and (2) perivascular drainage of Ab contribute to the different regional patterns of CAA in the mouse brain. Quantitative electron microscopy of the brains of 2-, 7-, and 23-month-old mice revealed significant age-related thickening of capillary basement membranes in cerebral cortex, hippocampus, and thalamus, but not in the striatum. Results from Western blotting and immunocytochemistry experiments showed a significant reduction in collagen IV in the cortex and hippocampus with age and a reduction in laminin and nidogen 2 in the cortex and striatum. Injection of soluble Ab into the hippocampus or thalamus showed an agerelated reduction in perivascular drainage from the hippocampus but not from the thalamus. The results of the study suggest that changes in vascular basement membranes and perivascular drainage with age differ between brain regions, in the mouse, in a manner that may help to explain the differential deposition of Ab in the brain in AD and may facilitate development of improved therapeutic strategies to remove Ab from the brain in AD.

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“…Collagen IV disrupts preformed Ab42 fibrils in vitro by inducing a structural transition from b-sheet to random structures in Ab42, which is the initially deposited species in the plaques and can serve as nucleation site for fibril formation by soluble Ab40 peptide [217].…”

Section: Collagens and Neurodegenerative Diseasesmentioning

confidence: 99%