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[PMID]:28844070
[Au] Autor:Banerjee G; Carare R; Cordonnier C; Greenberg SM; Schneider JA; Smith EE; Buchem MV; Grond JV; Verbeek MM; Werring DJ
[Ad] Endereço:Stroke Research Centre, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, UK.
[Ti] Título:The increasing impact of cerebral amyloid angiopathy: essential new insights for clinical practice.
[So] Source:J Neurol Neurosurg Psychiatry;88(11):982-994, 2017 Nov.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebral amyloid angiopathy (CAA) has never been more relevant. The last 5 years have seen a rapid increase in publications and research in the field, with the development of new biomarkers for the disease, thanks to advances in MRI, amyloid positron emission tomography and cerebrospinal fluid biomarker analysis. The inadvertent development of CAA-like pathology in patients treated with amyloid-beta immunotherapy for Alzheimer's disease has highlighted the importance of establishing how and why CAA develops; without this information, the use of these treatments may be unnecessarily restricted. Our understanding of the clinical and radiological spectrum of CAA has continued to evolve, and there are new insights into the independent impact that CAA has on cognition in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer's and other dementias. While the association between CAA and lobar intracerebral haemorrhage (with its high recurrence risk) is now well recognised, a number of management dilemmas remain, particularly when considering the use of antithrombotics, anticoagulants and statins. The Boston criteria for CAA, in use in one form or another for the last 20 years, are now being reviewed to reflect these new wide-ranging clinical and radiological findings. This review aims to provide a 5-year update on these recent advances, as well as a look towards future directions for CAA research and clinical practice.
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/efeitos adversos
Peptídeos beta-Amiloides/uso terapêutico
Biomarcadores/análise
Encéfalo/patologia
Angiopatia Amiloide Cerebral/induzido quimicamente
Angiopatia Amiloide Cerebral/patologia
Angiopatia Amiloide Cerebral Familiar/diagnóstico
Angiopatia Amiloide Cerebral Familiar/patologia
Seres Humanos
Imunoterapia
Neuroimagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Biomarkers)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170828
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2016-314697


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[PMID]:27989553
[Au] Autor:van Opstal AM; van Rooden S; van Harten T; Ghariq E; Labadie G; Fotiadis P; Gurol ME; Terwindt GM; Wermer MJH; van Buchem MA; Greenberg SM; van der Grond J
[Ad] Endereço:Department of Radiology, Leiden University Medical Center, Leiden, Netherlands. Electronic address: a.m.van_opstal@lumc.nl.
[Ti] Título:Cerebrovascular function in presymptomatic and symptomatic individuals with hereditary cerebral amyloid angiopathy: a case-control study.
[So] Source:Lancet Neurol;16(2):115-122, 2017 Feb.
[Is] ISSN:1474-4465
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous work suggests that impairments of cerebrovascular flow or reactivity might be early markers of cerebral amyloid angiopathy (CAA). Hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D) is a genetic form of CAA that can be diagnosed before the onset of clinical symptoms by DNA testing. We aimed to investigate whether haemodynamic measures are decreased in presymptomatic and symptomatic HCHWA-D mutation carriers compared with healthy controls. METHODS: In this case-control study, we included presymptomatic and symptomatic HCHWA-D mutation carriers diagnosed through genetic testing and recruited through the HCHWA-D patient association (Katwijk, Netherlands) and the outpatient clinic of the Department of Neurology of the Leiden University Medical Center (Leiden, Netherlands), and healthy controls. We measured regional cerebral blood flow (rCBF) using pseudo-continuous arterial spin labelling. Quantitative flow was measured by phase-contrast magnetic resonance angiography of the cerebropetal vessels. Vascular reactivity was established by measuring changes in blood-oxygen-level-dependent (BOLD) signal after visual stimulation. Data from presymptomatic and symptomatic individuals were compared with healthy controls using mixed-model regression analysis. FINDINGS: Between May 15, 2012, and December 22, 2015, we investigated cross-sectional imaging data from 27 HCHWA-D mutation carriers (12 presymptomatic and 15 symptomatic) and 33 healthy controls. Compared with controls, symptomatic HCHWA-D carriers had significantly decreased cortical grey matter rCBF in the occipital lobe (mean difference -11·1 mL/100 g per min, 95% CI -2·8 to -19·3; uncorrected p=0·010) and decreased flux in the basilar artery (mean difference -0·9 mL/s, 95% CI -1·5 to -0·2; uncorrected p=0·019). However, we noted no changes in rCBF and flux in presymptomatic carriers compared with controls. Vascular reactivity was significantly decreased in the occipital lobe in both presymptomatic (mean BOLD change 1·1% [SD 0·5], mean difference -0·4% change, 95% CI -0·7 to -0·2; p=0·001; mean time to baseline 10·1 s [SD 7·6], mean difference 4·6 s, 95% CI 0·4 to 8·8; p=0·032) and symptomatic carriers (mean BOLD change 0·4% [SD 0·1], mean difference -0·9%, 95% CI -1·1 to -0·6; p<0·0001; mean time to baseline 20·3 s [SD 8·4], mean difference 13·1 s, 95% CI 9·4 to 16·9; p<0·0001) compared with controls; however, the difference in mean time to peak was only significant for symptomatic carriers (mean difference 12·2 s, 95% CI 8·6 to 15·9; p<0·0001). INTERPRETATION: Our findings suggest that determination of vascular reactivity might be a useful biomarker for early detection of vascular amyloid pathology in sporadic CAA, and a biomarker of efficacy in future intervention trials. Our data indicate that vascular reactivity measurements might be useful for differential diagnosis in dementia to determine the vascular component. FUNDING: USA National Institutes of Health.
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral Familiar/diagnóstico por imagem
Angiopatia Amiloide Cerebral Familiar/fisiopatologia
Imagem por Ressonância Magnética/métodos
[Mh] Termos MeSH secundário: Adulto
Biomarcadores
Estudos de Casos e Controles
Estudos Transversais
Feminino
Heterozigoto
Seres Humanos
Angiografia por Ressonância Magnética/métodos
Masculino
Meia-Idade
Sintomas Prodrômicos
Marcadores de Spin
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Spin Labels)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE


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[PMID]:27834748
[Au] Autor:van Rooden S; van Opstal AM; Labadie G; Terwindt GM; Wermer MJ; Webb AG; Middelkoop HA; Greenberg SM; van der Grond J; van Buchem MA
[Ad] Endereço:From the C.J. Gorter Center for High-Field MRI (S.v.R., A.M.v.O., A.G.W., J.v.d.G., M.A.v.B.), Department of Radiology (S.v.R., A.M.v.O., G.L., A.G.W., J.v.d.G., M.A.v.B.), and Department of Neurology (G.M.T., M.J.H.W., H.A.M.M.), Leiden University Medical Center, The Netherlands; and Department of
[Ti] Título:Early Magnetic Resonance Imaging and Cognitive Markers of Hereditary Cerebral Amyloid Angiopathy.
[So] Source:Stroke;47(12):3041-3044, 2016 Dec.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Early markers for cerebral amyloid angiopathy are largely unknown. We aimed to identify which magnetic resonance imaging (MRI) (performed at 7 and 3T) and cognitive markers are an early sign in (pre) symptomatic subjects with hereditary cerebral hemorrhage with amyloidosis-Dutch type. METHODS: Twenty-seven DNA-proven Dutch-type mutation carriers (15 symptomatic and 12 presymptomatic) (mean age of 45.9 years) and 33 controls (mean age of 45.6 years) were included. 7T and 3T MRI was performed, cerebral amyloid angiopathy and small-vessel disease type MRI markers were estimated, and cognitive performance was assessed. Univariate general linear modeling analysis was used to assess the association between MRI markers and cognitive performance on the one hand and on the other, mutation status, adjusted for age, sex, and education. RESULTS: In symptomatic patients, all established cerebral amyloid angiopathy MRI markers (microbleeds, intracerebral hemorrhages, subarachnoid hemorrhages, superficial siderosis, microinfarcts, volume of white matter hyperintensities, and dilated perivascular spaces in centrum semiovale) were increased compared with controls (P<0.05). In presymptomatic subjects, the prevalence of microinfarcts and median volume of white matter hyperintensities were increased in comparison to controls (P<0.05). Symptomatic patients performed worse on all cognitive domains, whereas presymptomatic subjects did not show differences in comparison with controls (P<0.05). CONCLUSIONS: White matter hyperintensities and microinfarcts are more prevalent among presymptomatic subjects and precede cognitive and neuropsychiatric symptoms and intracerebral hemorrhages.
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral Familiar/diagnóstico
Hemorragia Cerebral/diagnóstico por imagem
Infarto Cerebral/diagnóstico por imagem
Disfunção Cognitiva/diagnóstico
Leucoaraiose/diagnóstico por imagem
Imagem por Ressonância Magnética/métodos
[Mh] Termos MeSH secundário: Adulto
Angiopatia Amiloide Cerebral Familiar/diagnóstico por imagem
Angiopatia Amiloide Cerebral Familiar/fisiopatologia
Seres Humanos
Meia-Idade
Sintomas Prodrômicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170609
[Lr] Data última revisão:
170609
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161112
[St] Status:MEDLINE


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[PMID]:27466465
[Au] Autor:Sekijima Y; Yazaki M; Oguchi K; Ezawa N; Yoshinaga T; Yamada M; Yahikozawa H; Watanabe M; Kametani F; Ikeda S
[Ad] Endereço:From the Departments of Medicine (Neurology and Rheumatology) (Y.S., M.Y., N.E., T.Y., S.-i.I.) and Brain Disease Research (M.Y.), Shinshu University School of Medicine; Institute for Biomedical Sciences (Y.S., M.Y., S.-i.I.), Shinshu University; Jisenkai Brain Imaging Research Center (Y.S., K.O.);
[Ti] Título:Cerebral amyloid angiopathy in posttransplant patients with hereditary ATTR amyloidosis.
[So] Source:Neurology;87(8):773-81, 2016 Aug 23.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the prevalence and clinical features of posttransplant CNS symptoms in patients with hereditary ATTR amyloidosis and their Pittsburgh compound B (PiB)-PET imaging correlates. METHODS: We monitored prevalence and type of CNS symptoms in 53 consecutive posttransplant patients with hereditary ATTR amyloidosis. (11)C-PiB-PET was performed in 15 patients with various disease durations. We also analyzed pathologic and biochemical characteristics of ATTR amyloid deposition in the brain of a posttransplant patient. RESULTS: Transient focal neurologic episodes (TFNEs) attributed to ATTR-type cerebral amyloid angiopathy (CAA) were found in 11.3% of posttransplant hereditary ATTR amyloidosis patients. TFNE occurred on average 16.8 years after onset of the disease. Patients with longer duration of illness (≥10 years) showed increased (11)C-PiB retention in the brain. The (11)C-PiB accumulation pattern in hereditary ATTR amyloidosis was unique and different from those in Alzheimer disease or Aß-type CAA. In the autopsy case, ATTR amyloid deposition was mainly localized to leptomeningeal vessels and leptomeninges of the brain. Amyloid fibrils in the brain were almost completely composed of variant transthyretin (TTR). CONCLUSIONS: TFNE due to ATTR-type CAA occurred frequently in posttransplant patients with long disease durations. (11)C-PiB-PET is a useful diagnostic tool for ATTR-type CAA. ATTR amyloid deposition in the CNS, as measured by PiB-PET, was detected approximately 10 years before onset of TFNE.
[Mh] Termos MeSH primário: Compostos de Anilina
Doenças do Sistema Nervoso Central/etiologia
Angiopatia Amiloide Cerebral Familiar/complicações
Transplante de Fígado/métodos
Tomografia por Emissão de Pósitrons/métodos
Pré-Albumina/metabolismo
Tiazóis
[Mh] Termos MeSH secundário: Doenças do Sistema Nervoso Central/metabolismo
Doenças do Sistema Nervoso Central/fisiopatologia
Angiopatia Amiloide Cerebral Familiar/metabolismo
Angiopatia Amiloide Cerebral Familiar/cirurgia
Feminino
Seres Humanos
Masculino
Meia-Idade
Pré-Albumina/genética
Estudos Retrospectivos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole); 0 (Aniline Compounds); 0 (Prealbumin); 0 (Thiazoles)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003001


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[PMID]:27245348
[Au] Autor:Bersano A; Markus HS; Quaglini S; Arbustini E; Lanfranconi S; Micieli G; Boncoraglio GB; Taroni F; Gellera C; Baratta S; Penco S; Mosca L; Grasso M; Carrera P; Ferrari M; Cereda C; Grieco G; Corti S; Ronchi D; Bassi MT; Obici L; Parati EA; Pezzini A; De Lodovici ML; Verrengia EP; Bono G; Mazucchelli F; Zarcone D; Calloni MV; Perrone P; Bordo BM; Colombo A; Padovani A; Cavallini A; Beretta S; Ferrarese C; Motto C; Agostoni E; Molini G; Sasanelli F; Corato M; Marcheselli S; Sessa M; Comi G; Checcarelli N; Guidotti M; Uccellini D; Capitani E; Tancredi L; Arnaboldi M; Lombardia GENS Group*
[Ad] Endereço:From the Department of Cerebrovascular Disease, IRCCS Foundation Carlo Besta Neurological Institute, Milan, Italy (A.B., G.B.B., E.A.P., N.T.); Stroke Research Group, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom (H.S.M.); Department of Bio-Medical Informat
[Ti] Título:Clinical Pregenetic Screening for Stroke Monogenic Diseases: Results From Lombardia GENS Registry.
[So] Source:Stroke;47(7):1702-9, 2016 Jul.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Lombardia GENS is a multicentre prospective study aimed at diagnosing 5 single-gene disorders associated with stroke (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, Fabry disease, MELAS [mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes], hereditary cerebral amyloid angiopathy, and Marfan syndrome) by applying diagnostic algorithms specific for each clinically suspected disease METHODS: We enrolled a consecutive series of patients with ischemic or hemorrhagic stroke or transient ischemic attack admitted in stroke units in the Lombardia region participating in the project. Patients were defined as probable when presenting with stroke or transient ischemic attack of unknown etiopathogenic causes, or in the presence of <3 conventional vascular risk factors or young age at onset, or positive familial history or of specific clinical features. Patients fulfilling diagnostic algorithms specific for each monogenic disease (suspected) were referred for genetic analysis. RESULTS: In 209 patients (57.4±14.7 years), the application of the disease-specific algorithm identified 227 patients with possible monogenic disease. Genetic testing identified pathogenic mutations in 7% of these cases. Familial history of stroke was the only significant specific feature that distinguished mutated patients from nonmutated ones. The presence of cerebrovascular risk factors did not exclude a genetic disease. CONCLUSIONS: In patients prescreened using a clinical algorithm for monogenic disorders, we identified monogenic causes of events in 7% of patients in comparison to the 1% to 5% prevalence reported in previous series.
[Mh] Termos MeSH primário: CADASIL/genética
Angiopatia Amiloide Cerebral Familiar/genética
Doença de Fabry/genética
Testes Genéticos
Síndrome MELAS/genética
Síndrome de Marfan/genética
Acidente Vascular Cerebral/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
CADASIL/complicações
Angiopatia Amiloide Cerebral Familiar/complicações
Análise Mutacional de DNA
Doença de Fabry/complicações
Feminino
Seres Humanos
Síndrome MELAS/complicações
Masculino
Síndrome de Marfan/complicações
Meia-Idade
Mutação
Sistema de Registros
Acidente Vascular Cerebral/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160602
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.115.012281


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[PMID]:27000221
[Au] Autor:Zarranz JJ; Fernandez-Martinez M; Rodriguez O; Mateos B; Iglesias S; Baron JC
[Ad] Endereço:Department of Neurology, Hospital de Cruces, Basque Country School of Medicine, Baracaldo, Vizcaya, Spain.
[Ti] Título:Iowa APP mutation-related hereditary cerebral amyloid angiopathy (CAA): A new family from Spain.
[So] Source:J Neurol Sci;363:55-6, 2016 Apr 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral Familiar
Saúde da Família
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160322
[Lr] Data última revisão:
160322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160323
[St] Status:MEDLINE


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[PMID]:26661731
[Au] Autor:Montañola A; de Retana SF; López-Rueda A; Merino-Zamorano C; Penalba A; Fernández-Álvarez P; Rodríguez-Luna D; Malagelada A; Pujadas F; Montaner J; Hernández-Guillamon M
[Ad] Endereço:Neurovascular Research Laboratory, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d'Hebron 119-129, 08035, Barcelona, Spain.
[Ti] Título:ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy.
[So] Source:Neuromolecular Med;18(1):99-108, 2016 Mar.
[Is] ISSN:1559-1174
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The involvement of apolipoproteins, such as the ApoE4 isoform, in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) highlights the fact that certain lipid carriers may participate in soluble ß-amyloid (Aß) transport. Our general aim was to characterize the soluble levels of the apolipoproteins apoE, apoA1 and apoJ/clusterin and their genotype status in patients with CAA. We analyzed the genotypes frequency of APOA1 (rs5069, rs670), CLU (rs11136000, rs1532278, rs7012010, rs9331888) and APOE (rs429358, rs7412) in a cohort of patients with CAA-associated intracerebral hemorrhage (ICH) (n = 59) and compared the results with those from hypertension-associated ICH (n = 42), AD patients (n = 73) and controls (n = 88). In a subgroup of patients, we also determined the plasma concentrations of apoE, apoA1 and apoJ/clusterin. We found increased plasma apoJ/clusterin levels in CAA patients compared to AD patients or controls after adjusting for sex and age (CAA vs. controls, p = 0.033; CAA vs. AD, p = 0.013). ApoA1 levels were not altered between groups, although a strong correlation was observed between plasma Aß(1-40) and apoA1 among CAA patients (r = 0.583, p = 0.007). Regarding plasma apoE concentration, a robust association between circulating levels and genotype status was confirmed (p < 0.001). Whereas the APOE4 frequency was higher in AD (p < 0.001) and CAA (p = 0.013), the APOA1 and CLU genotypes were not different among groups. In the CAA cohort, the risk-linked CLU variant (C) rs11136000 was associated with white matter hyperintensities (p = 0.045) and the presence of lobar microbleeds (p = 0.023) on MRI. In summary, our findings suggest that apoA1 may act as a physiological transporter of Aß(1-40) and that apoJ/clusterin appears to be a chaperone related to distinctive lesions in CAA brains.
[Mh] Termos MeSH primário: Apolipoproteína A-I/genética
Apolipoproteínas E/genética
Angiopatia Amiloide Cerebral/genética
Clusterina/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/sangue
Doença de Alzheimer/genética
Apolipoproteína A-I/sangue
Apolipoproteínas E/sangue
Angiopatia Amiloide Cerebral/sangue
Angiopatia Amiloide Cerebral/complicações
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Angiopatia Amiloide Cerebral Familiar/sangue
Angiopatia Amiloide Cerebral Familiar/complicações
Angiopatia Amiloide Cerebral Familiar/diagnóstico por imagem
Angiopatia Amiloide Cerebral Familiar/genética
Hemorragia Cerebral/etiologia
Clusterina/sangue
Feminino
Frequência do Gene
Genótipo
Seres Humanos
Hipertensão/sangue
Hipertensão/complicações
Hipertensão/genética
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Substância Branca/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (ApoE protein, human); 0 (Apolipoprotein A-I); 0 (Apolipoproteins E); 0 (CLU protein, human); 0 (Clusterin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.1007/s12017-015-8381-7


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[PMID]:26115583
[Au] Autor:Osk Snorradottir A; Isaksson HJ; Kaeser SA; Skodras AA; Olafsson E; Palsdottir A; Thor Bragason B
[Ad] Endereço:Institute for Experimental Pathology at Keldur, University of Iceland, Reykjavik, Iceland.
[Ti] Título:Parenchymal cystatin C focal deposits and glial scar formation around brain arteries in Hereditary Cystatin C Amyloid Angiopathy.
[So] Source:Brain Res;1622:149-62, 2015 Oct 05.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hereditary Cystatin C Amyloid Angiopathy (HCCAA) is an amyloid disorder in Icelandic families caused by an autosomal dominant mutation in the cystatin C gene. Mutant cystatin C forms amyloid deposits in brain arteries and arterioles which are associated with changes in the arterial wall structure, notably deposition of extracellular matrix proteins. In this post-mortem study we examined the neuroinflammatory response relative to the topographical distribution of cystatin C deposition, and associated haemorrhages, in the leptomeninges, cerebrum, cerebellum, thalamus, and midbrain of HCCAA patients. Cystatin C was deposited in all brain areas, grey and white matter alike, most prominently in arteries and arterioles; capillaries and veins were not, or minimally, affected. We also observed perivascular deposits and parenchymal focal deposits proximal to affected arteries. This study shows for the first time, that cystatin C does not exclusively form CAA and perivascular amyloid but also focal deposits in the brain parenchyma. Haemorrhages were observed in all patients and occurred in all brain areas, variable between patients. Microinfarcts were observed in 34.6% of patients. The neuroinflammatory response was limited to the close vicinity of affected arteries and perivascular as well as parenchymal focal deposits. Taken together with previously reported arterial accumulation of extracellular matrix proteins in HCCAA, our results indicate that the central nervous system pathology of HCCAA is characterised by the formation of a glial scar within and around affected arteries.
[Mh] Termos MeSH primário: Encéfalo/patologia
Angiopatia Amiloide Cerebral Familiar/patologia
Cicatriz/patologia
Cistatina C/metabolismo
Neuroglia/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Arteríolas/metabolismo
Arteríolas/patologia
Encéfalo/irrigação sanguínea
Encéfalo/metabolismo
Infarto Encefálico/patologia
Infarto Encefálico/fisiopatologia
Angiopatia Amiloide Cerebral Familiar/genética
Angiopatia Amiloide Cerebral Familiar/fisiopatologia
Artérias Cerebrais/patologia
Cicatriz/metabolismo
Cistatina C/genética
Proteínas de Ligação a DNA/metabolismo
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Masculino
Meia-Idade
Neuroimunomodulação/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (CST3 protein, human); 0 (Cystatin C); 0 (DNA-Binding Proteins); 0 (Glial Fibrillary Acidic Protein)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:150908
[Lr] Data última revisão:
150908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150628
[St] Status:MEDLINE


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[PMID]:26104569
[Au] Autor:Iwanowski P; Kozubski W; Losy J
[Ad] Endereço:Department of Neurology, Poznan University School of Medicine, Poland; Department of Clinical Neuroimmunology, Chair of Neurology, Poznan University School of Medicine, Poland. Electronic address: bluep@op.pl.
[Ti] Título:Iowa-type hereditary cerebral amyloid angiopathy in a Polish family.
[So] Source:J Neurol Sci;356(1-2):202-4, 2015 Sep 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral Familiar
Saúde da Família
[Mh] Termos MeSH secundário: Adulto
Angiopatia Amiloide Cerebral Familiar/genética
Angiopatia Amiloide Cerebral Familiar/patologia
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Polônia
Prótons
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protons)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160722
[Lr] Data última revisão:
160722
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150625
[St] Status:MEDLINE


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[PMID]:25957407
[Au] Autor:Cantlon A; Frigerio CS; Freir DB; Boland B; Jin M; Walsh DM
[Ad] Endereço:From the Laboratory for Neurodegenerative Research, School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Republic of Ireland and the Laboratory for Neurodegenerative Research, Ann Romney Center for Neurologic Diseases, Brigham and Women's Ho
[Ti] Título:The Familial British Dementia Mutation Promotes Formation of Neurotoxic Cystine Cross-linked Amyloid Bri (ABri) Oligomers.
[So] Source:J Biol Chem;290(27):16502-16, 2015 Jul 03.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Familial British dementia (FBD) is an inherited neurodegenerative disease believed to result from a mutation in the BRI2 gene. Post-translational processing of wild type BRI2 and FBD-BRI2 result in the production of a 23-residue long Bri peptide and a 34-amino acid long ABri peptide, respectively, and ABri is found deposited in the brains of individuals with FBD. Similarities in the neuropathology and clinical presentation shared by FBD and Alzheimer disease (AD) have led some to suggest that ABri and the AD-associated amyloid ß-protein (Aß) are molecular equivalents that trigger analogous pathogenic cascades. But the sequences and innate properties of ABri and Aß are quite different, notably ABri contains two cysteine residues that can form disulfide bonds. Thus we sought to determine whether ABri was neurotoxic and if this activity was regulated by oxidation and/or aggregation. Crucially, the type of oxidative cross-linking dramatically influenced both ABri aggregation and toxicity. Cyclization of Bri and ABri resulted in production of biologically inert monomers that showed no propensity to assemble, whereas reduced ABri and reduced Bri aggregated forming thioflavin T-positive amyloid fibrils that lacked significant toxic activity. ABri was more prone to form inter-molecular disulfide bonds than Bri and the formation of covalently stabilized ABri oligomers was associated with toxicity. These results suggest that extension of the C-terminal of Bri causes a shift in the type of disulfide bonds formed and that structures built from covalently cross-linked oligomers can interact with neurons and compromise their function and viability.
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral Familiar/genética
Cistina/química
Glicoproteínas de Membrana/química
Glicoproteínas de Membrana/genética
Mutação
Neurotoxinas/química
Neurotoxinas/genética
[Mh] Termos MeSH secundário: Amiloide
Animais
Angiopatia Amiloide Cerebral Familiar/metabolismo
Angiopatia Amiloide Cerebral Familiar/fisiopatologia
Cistina/genética
Cistina/metabolismo
Seres Humanos
Potenciação de Longa Duração
Masculino
Glicoproteínas de Membrana/metabolismo
Glicoproteínas de Membrana/toxicidade
Camundongos
Camundongos Endogâmicos C57BL
Neurotoxinas/metabolismo
Neurotoxinas/toxicidade
Oxirredução
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid); 0 (ITM2B protein, human); 0 (Membrane Glycoproteins); 0 (Neurotoxins); 48TCX9A1VT (Cystine)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150510
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.652263



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