Interaction between β-amyloid protein and heparan sulfate proteoglycans from the cerebral capillary basement membrane in Alzheimer’s disease

Shimizu, Hajime; Ghazizadeh, Mohammad; Satō, Shigeru; Oguro, Tatsuo; Kawanami, Oichi

doi:10.1016/j.jocn.2008.04.009

Cited by 39 publications

(31 citation statements)

References 15 publications

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“…Heparan sulfate proteoglycans such as fibronectin and perlecan provide stability and flexibility to the basement membrane, accelerating the aggregation of Ab by high-affinity interactions (Castillo et al, 1997;Cotman et al, 2000). In AD brains, the levels of heparan sulfate proteoglycans are increased compared with agematched controls (Berzin et al, 2000;Shimizu et al, 2009). In this study in the mouse, we found that the levels of collagen IV was significantly decreased in the cortex and in the hippocampus, but not in the striatum and thalamus of aged mice.…”

Section: Discussionmentioning

confidence: 55%

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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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Section: Discussionmentioning

confidence: 55%

“…Vacuolization, reduplication, and thickening of capillary basement membranes have also been shown to occur in the human aged and AD brain (Perlmutter, 1994;Shimizu et al, 2009).…”

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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“…In terms of the specific locations of changes in HSPGs, one study found an increase in HSPGs in the hippocampus of subjects with AD, suggesting a role for HSPGs in AD pathogenesis [62]. Another study of HS expression in the hippocampus of aged (mean age 66 years) versus adult (mean age 28 years) subjects demonstrated structural changes in HS in the hippocampus of aged subjects.…”

Section: Discussionmentioning

confidence: 99%

Decreased Expression of Sulfatase 2 in the Brains of Alzheimer’s Disease Patients: Implications for Regulation of Neuronal Cell Signaling

Roberts

Kang

et al. 2017

ADR

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Background The human sulfatase 1 (SULF1) and sulfatase 2 (SULF2) genes modulate cell signaling and homeostasis in many tissues. Gene expression analyses have implicated SULF2 in disease pathogenesis, including Alzheimer’s disease (AD), but changes in brain SULF2 expression have not been directly established. Objective To investigate the expression of SULF1 and SULF2 in brain tissues from AD cases and cognitively normal controls. Methods Autopsy tissue from AD cases (n = 20) and age-and gender-matched cognitively normal controls (n = 20) were identified from the Mayo Clinic Alzheimer’s Disease Patient Registry neuropathology database. Tissue slides were stained for SULF1 and SULF2 protein expression in the hippocampus and frontal lobe and an expression score computed from the proportion of cells stained and the intensity of staining (range 0 [no expression] to 9 [marked expression]). Results SULF2 expression was reduced in AD cases. Compared to cognitively normal controls, SULF2 expression in AD cases was significantly decreased in the hippocampal Cornu Ammonis (CA) (mean score of 6.5 in cases versus 8.3 in controls; p = 0.003), in the gray matter of the parahippocampal gyrus (5.6 in cases versus 7.6 in controls; p = 0.003), and in the frontal lobe gray matter (5.4 in cases versus 7.4 in controls; p = 0.002). There was no difference in SULF1 expression in the hippocampus or frontal lobe of AD cases and controls. As expected there were no differences in SULF1 or SULF2 expression in white matter in AD cases compared to cognitively normal controls. Conclusion Decresed SULF2 in specific regions of the brain occurs in AD.

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“…Thickening, splitting, duplication, and the presence of abnormal inclusions in the CVBM have been reported in the brains of aged animals and humans and to a greater degree in the AD brain (Perlmutter, 1994; Kalaria, 1996; Farkas and Luiten, 2001; Shimizu et al, 2009). Thickening of the CVBM in both rodents and humans appears to be most predominant in brain areas that are susceptible to AD and CAA pathology (Zarow et al, 1997; Hawkes et al, 2013) and precedes CAA onset in TGF-β transgenic mice (Wyss-Coray et al, 2000).…”

Section: Role Of Cvbm and Perivascular Drainage In Caamentioning

confidence: 97%

“…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). Conversely, the levels of HSPGs were increased in AD brains (Berzin et al, 2000; Shimizu et al, 2009). Similar alterations have also been observed in the levels of collagen IV, laminin, nidogen 2, fibronectin, and perlecan in CAA-vulnerable brain regions of aged mice (Hawkes et al, 2013).…”

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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Interaction between β-amyloid protein and heparan sulfate proteoglycans from the cerebral capillary basement membrane in Alzheimer’s disease

Cited by 39 publications

References 15 publications

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

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

Decreased Expression of Sulfatase 2 in the Brains of Alzheimer’s Disease Patients: Implications for Regulation of Neuronal Cell Signaling

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

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