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[PMID]:28457579
[Au] Autor:Jacquemont T; De Vico Fallani F; Bertrand A; Epelbaum S; Routier A; Dubois B; Hampel H; Durrleman S; Colliot O; Alzheimer's Disease Neuroimaging Initiative
[Ad] Endereço:Inserm, U1127, Paris, France; CNRS, UMR 7225 ICM, Paris, France; Sorbonne Universités, UPMC Univ Paris 06, UMR S 1127, Paris, France; Institut du Cerveau et de la Moelle épinière, ICM, Paris, France; Inria, Aramis project-team, Centre de Recherche de Paris, France; Département de Biologie, Ecole nor
[Ti] Título:Amyloidosis and neurodegeneration result in distinct structural connectivity patterns in mild cognitive impairment.
[So] Source:Neurobiol Aging;55:177-189, 2017 Jul.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alzheimer's disease (AD) is increasingly considered as a disconnection syndrome. Previous studies of the structural connectome in early AD stages have focused on mild cognitive impaired subjects (MCI), considering them as a homogeneous group. We studied 168 subjects from the Alzheimer's Disease Neuroimaging Initiative database (116 MCI and 52 cognitively normal subjects). Biomarker-based stratification using amyloid biomarkers (AV45 PET) and neurodegeneration biomarkers (MRI and FDG PET) led to 4 subgroups based on amyloid positivity (A+/-) and neurodegeneration positivity (N+/-): A-N-, A+N-, A-N+, and A+N+. Using diffusion MRI, we showed that both MCI A-N+ and MCI A+N+ subjects displayed an alteration of the white matter in the fornix and a significant bihemispheric network of decreased connections. These network alterations in MCI A+N+ are stronger and more focal than those of MCI A-N+. Only MCI A+N+ subjects exhibited specific changes in hippocampal connectivity and an AD-like alteration pattern. Our results indicate that the connectome disintegration pattern of MCI subgroups differ with respect to brain amyloid and neurodegeneration. Each of these 2 AD biomarkers induces a connectome alteration that is maximal when they coexist.
[Mh] Termos MeSH primário: Doença de Alzheimer/complicações
Angiopatia Amiloide Cerebral/complicações
Cognição/fisiologia
Disfunção Cognitiva/etiologia
Disfunção Cognitiva/psicologia
Degeneração Neural/complicações
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/diagnóstico por imagem
Biomarcadores
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Disfunção Cognitiva/diagnóstico por imagem
Disfunção Cognitiva/patologia
Conectoma
Imagem de Difusão por Ressonância Magnética
Feminino
Hipocampo/diagnóstico por imagem
Hipocampo/fisiopatologia
Seres Humanos
Masculino
Meia-Idade
Degeneração Neural/diagnóstico por imagem
Tomografia por Emissão de Pósitrons
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28963121
[Au] Autor:Jäkel L; Van Nostrand WE; Nicoll JAR; Werring DJ; Verbeek MM
[Ad] Endereço:Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer Centre, Nijmegen, The Netherlands.
[Ti] Título:Animal models of cerebral amyloid angiopathy.
[So] Source:Clin Sci (Lond);131(19):2469-2488, 2017 Oct 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebral amyloid angiopathy (CAA), due to vascular amyloid ß (Aß) deposition, is a risk factor for intracerebral haemorrhage and dementia. CAA can occur in sporadic or rare hereditary forms, and is almost invariably associated with Alzheimer's disease (AD). Experimental (animal) models are of great interest in studying mechanisms and potential treatments for CAA. Naturally occurring animal models of CAA exist, including cats, dogs and non-human primates, which can be used for longitudinal studies. However, due to ethical considerations and low throughput of these models, other animal models are more favourable for research. In the past two decades, a variety of transgenic mouse models expressing the human Aß precursor protein (APP) has been developed. Many of these mouse models develop CAA in addition to senile plaques, whereas some of these models were generated specifically to study CAA. In addition, other animal models make use of a second stimulus, such as hypoperfusion or hyperhomocysteinemia (HHcy), to accelerate CAA. In this manuscript, we provide a comprehensive review of existing animal models for CAA, which can aid in understanding the pathophysiology of CAA and explore the response to potential therapies.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Encéfalo/metabolismo
Angiopatia Amiloide Cerebral/metabolismo
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/genética
Animais
Encéfalo/patologia
Encéfalo/fisiopatologia
Angiopatia Amiloide Cerebral/genética
Angiopatia Amiloide Cerebral/patologia
Angiopatia Amiloide Cerebral/fisiopatologia
Modelos Animais de Doenças
Predisposição Genética para Doença
Seres Humanos
Camundongos Transgênicos
Fenótipo
Placa Amiloide
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (APP protein, human); 0 (Amyloid beta-Protein Precursor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170033


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[PMID]:28855406
[Au] Autor:Charidimou A; Farid K; Baron JC
[Ad] Endereço:From the Massachusetts General Hospital (A.C.), Stroke Research Center, Harvard Medical School, Boston; Department of Nuclear Medicine (K.F.), Martinique University Hospital, Fort-de-France, French West Indies; and Department of Neurology (J.-C.B.), Centre Hospitalier Sainte Anne, Inserm U894, Sorbonne Paris Cité, France. andreas.charidimou.09@ucl.ac.uk.
[Ti] Título:Amyloid-PET in sporadic cerebral amyloid angiopathy: A diagnostic accuracy meta-analysis.
[So] Source:Neurology;89(14):1490-1498, 2017 Oct 03.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To perform a meta-analysis synthesizing evidence of the value and accuracy of amyloid-PET in diagnosing patients with sporadic cerebral amyloid angiopathy (CAA). METHODS: In a PubMed systematic literature search, we identified all case-control studies with extractable data relevant for the sensitivity and specificity of amyloid-PET positivity in symptomatic patients with CAA (cases) vs healthy participants or patients with spontaneous deep intracerebral hemorrhage (ICH) (control groups). Using a hierarchical (multilevel) logistic regression model, we calculated pooled diagnostic test accuracy. RESULTS: Seven studies, including 106 patients with CAA (>90% with probable CAA) and 151 controls, were eligible and included in the meta-analysis. The studies were of moderate to high quality and varied in several methodological aspects, including definition of PET-positive and PET-negative cases and relevant cutoffs. The sensitivity of amyloid-PET for CAA diagnosis ranged from 60% to 91% and the specificity from 56% to 90%. The overall pooled sensitivity was 79% (95% confidence interval [CI] 62-89) and specificity was 78% (95% CI 67-86) for CAA diagnosis. A predefined subgroup analysis of studies restricted to symptomatic patients presenting with lobar ICH CAA (n = 58 vs 86 controls) resulted in 79% sensitivity (95% CI 61-90%) and 84% specificity (95% CI 65-93%). In prespecified bivariate diagnostic accuracy meta-analysis of 2 studies using F-florbetapir-PET, the sensitivity for CAA-ICH diagnosis was 90% (95% CI 76-100%) and specificity was 88% (95% CI 74-100%). CONCLUSIONS: Amyloid-PET appears to have moderate to good diagnostic accuracy in differentiating patients with probable CAA from cognitively normal healthy controls or patients with deep ICH. Given that amyloid-PET labels both cerebrovascular and parenchymal amyloid, a negative scan might be useful to rule out CAA in the appropriate clinical setting.
[Mh] Termos MeSH primário: Amiloide/metabolismo
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Angiopatia Amiloide Cerebral/metabolismo
Tomografia por Emissão de Pósitrons
[Mh] Termos MeSH secundário: Bases de Dados Factuais/estatística & dados numéricos
Feminino
Fluordesoxiglucose F18/metabolismo
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Amyloid); 0Z5B2CJX4D (Fluorodeoxyglucose F18)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004539


  4 / 1411 MEDLINE  
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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]:28838368
[Au] Autor:DeSimone CV; Graff-Radford J; El-Harasis MA; Rabinstein AA; Asirvatham SJ; Holmes DR
[Ad] Endereço:Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.
[Ti] Título:Cerebral Amyloid Angiopathy: Diagnosis, Clinical Implications, and Management Strategies in Atrial Fibrillation.
[So] Source:J Am Coll Cardiol;70(9):1173-1182, 2017 Aug 29.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:With an aging population, clinicians are more frequently encountering patients with atrial fibrillation who are also at risk of intracerebral hemorrhage due to cerebral amyloid angiopathy, the result of ß-amyloid deposition in cerebral vessels. Cerebral amyloid angiopathy is common among elderly patients, and is associated with an increased risk of intracerebral bleeding, especially with the use of anticoagulation. Despite this association, this entity is absent in current risk-benefit analysis models, which may result in underestimation of the chance of bleeding in the subset of patients with this disease. Determining the presence and burden of cerebral amyloid angiopathy is particularly important when planning to start or restart anticoagulation after an intracerebral hemorrhage. Given the lack of randomized trial data to guide management strategies, we discuss a heart-brain team approach that includes clinician-patient shared decision making for the use of pharmacologic and nonpharmacologic approaches to diminish stroke risk.
[Mh] Termos MeSH primário: Fibrilação Atrial
Angiopatia Amiloide Cerebral
Gerenciamento Clínico
[Mh] Termos MeSH secundário: Fibrilação Atrial/diagnóstico
Fibrilação Atrial/etiologia
Fibrilação Atrial/terapia
Angiopatia Amiloide Cerebral/complicações
Angiopatia Amiloide Cerebral/diagnóstico
Angiopatia Amiloide Cerebral/terapia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


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[PMID]:28706123
[Au] Autor:Marinescu M; Sun L; Fatar M; Neubauer A; Schad L; van Ryn J; Lehmann L; Veltkamp R
[Ad] Endereço:From the Division of Brain Sciences, Imperial College London, United Kingdom (M.M., R.V.); Departments of Neurology (M.M., L.S., R.V.) and Cardiology (L.L.), University of Heidelberg, Germany; Department of Neurology, Medical Faculty Mannheim (M.F.), Computer Assisted Clinical Medicine (A.N., L.S.),
[Ti] Título:Cerebral Microbleeds in Murine Amyloid Angiopathy: Natural Course and Anticoagulant Effects.
[So] Source:Stroke;48(8):2248-2254, 2017 Aug.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Cerebral microbleeds (CMBs) predispose patients to intracerebral hemorrhage. Preclinical models to examine the effects of antithrombotic treatments on the development of clinically overt intracerebral hemorrhage are needed. We examined the natural course of CMB development and the effects of long-term anticoagulation with warfarin or dabigatran on cerebral micro- and macrohemorrhage in mice overexpressing the APP23 (amyloid precursor protein). METHODS: Repeated susceptibility-weighted magnetic resonance imaging was performed in APP23 mice at the age of 18 and 21 months, respectively. After establishing stable long-term anticoagulation effects of warfarin and dabigatran on number and total volume of CMBs, the outcome parameters were compared with nonanticoagulated control. RESULTS: CMBs were equally located in lobar and deep brain regions, and number and total volume of CMBs increased over time. Anticoagulation with either warfarin or dabigatran did not increase CMBs in APP23 significantly. Mice treated with warfarin numerically had a higher mortality (nonanticoagulated: 31%; dabigatran: 35% versus warfarin: 55%; =0.21). In postmortem brains of prematurely dying animals warfarin caused significantly more frequently large intracerebral hemorrhage than control and dabigatran. CONCLUSIONS: Anticoagulation with warfarin or dabigatran for 3 to 4 months does not promote the formation of CMBs in aged APP23 mice. Nevertheless, warfarin but not dabigatran is associated with a higher risk of extensive intracerebral hemorrhage, suggesting that this model may allow preclinical safety evaluation of antithrombotic therapies.
[Mh] Termos MeSH primário: Anticoagulantes/uso terapêutico
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Angiopatia Amiloide Cerebral/tratamento farmacológico
Hemorragia Cerebral/diagnóstico por imagem
Hemorragia Cerebral/tratamento farmacológico
Microvasos/diagnóstico por imagem
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/genética
Animais
Anticoagulantes/farmacologia
Angiopatia Amiloide Cerebral/genética
Hemorragia Cerebral/genética
Feminino
Imagem por Ressonância Magnética/tendências
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microvasos/efeitos dos fármacos
Distribuição Aleatória
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Anticoagulants)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017994


  7 / 1411 MEDLINE  
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[PMID]:28700676
[Au] Autor:Samarasekera N; Rodrigues MA; Toh PS; Al-Shahi R
[Ad] Endereço:Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom.
[Ti] Título:Imaging features of intracerebral hemorrhage with cerebral amyloid angiopathy: Systematic review and meta-analysis.
[So] Source:PLoS One;12(7):e0180923, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We sought to summarize Computed Tomography (CT)/Magnetic Resonance Imaging (MRI) features of intracerebral hemorrhage (ICH) associated with cerebral amyloid angiopathy (CAA) in published observational radio-pathological studies. METHODS: In November 2016, two authors searched OVID Medline (1946-), Embase (1974-) and relevant bibliographies for studies of imaging features of lobar or cerebellar ICH with pathologically proven CAA ("CAA-associated ICH"). Two authors assessed studies' diagnostic test accuracy methodology and independently extracted data. RESULTS: We identified 22 studies (21 cases series and one cross-sectional study with controls) of CT features in 297 adults, two cross-sectional studies of MRI features in 81 adults and one study which reported both CT and MRI features in 22 adults. Methods of CAA assessment varied, and rating of imaging features was not masked to pathology. The most frequently reported CT features of CAA-associated ICH in 21 case series were: subarachnoid extension (pooled proportion 82%, 95% CI 69-93%, I2 = 51%, 12 studies) and an irregular ICH border (64%, 95% CI 32-91%, I2 = 85%, five studies). CAA-associated ICH was more likely to be multiple on CT than non-CAA ICH in one cross-sectional study (CAA-associated ICH 7/41 vs. non-CAA ICH 0/42; χ2 = 7.8, p = 0.005). Superficial siderosis on MRI was present in 52% of CAA-associated ICH (95% CI 39-65%, I2 = 35%, 3 studies). CONCLUSIONS: Subarachnoid extension and an irregular ICH border are common imaging features of CAA-associated ICH, but methodologically rigorous diagnostic test accuracy studies are required to determine the sensitivity and specificity of these features.
[Mh] Termos MeSH primário: Angiopatia Amiloide Cerebral/diagnóstico
Hemorragia Cerebral/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Angiopatia Amiloide Cerebral/metabolismo
Angiopatia Amiloide Cerebral/patologia
Hemorragia Cerebral/metabolismo
Hemorragia Cerebral/patologia
Estudos Transversais
Seres Humanos
Imagem por Ressonância Magnética
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180923


  8 / 1411 MEDLINE  
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[PMID]:28677558
[Au] Autor:DeSimone CV; Graff-Radford J; El-Harasis MA; Rabinstein AA; Asirvatham SJ; Holmes DR
[Ad] Endereço:Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
[Ti] Título:Cerebral amyloid angiopathy and implications for atrial fibrillation management.
[So] Source:Lancet;390(10089):9-11, 2017 07 01.
[Is] ISSN:1474-547X
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Fibrilação Atrial
Angiopatia Amiloide Cerebral/complicações
Angiopatia Amiloide Cerebral/epidemiologia
[Mh] Termos MeSH secundário: Idoso
Anticoagulantes/uso terapêutico
Fibrilação Atrial/tratamento farmacológico
Encéfalo
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE


  9 / 1411 MEDLINE  
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[PMID]:28667120
[Au] Autor:Salvadores N; Searcy JL; Holland PR; Horsburgh K
[Ad] Endereço:Centre for Neuroregeneration, University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh EH164SB, U.K.
[Ti] Título:Chronic cerebral hypoperfusion alters amyloid-ß peptide pools leading to cerebral amyloid angiopathy, microinfarcts and haemorrhages in Tg-SwDI mice.
[So] Source:Clin Sci (Lond);131(16):2109-2123, 2017 Aug 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebral hypoperfusion is an early feature of Alzheimer's disease (AD) that influences the progression from mild cognitive impairment to dementia. Understanding the mechanism is of critical importance in the search for new effective therapies. We hypothesized that cerebral hypoperfusion promotes the accumulation of amyloid-ß (Aß) and degenerative changes in the brain and is a potential mechanism contributing to development of dementia. To address this, we studied the effects of chronic cerebral hypoperfusion induced by bilateral carotid artery stenosis on Aß peptide pools in a transgenic mouse model of AD (transgenic mice with Swedish, Dutch and Iowa mutations in human amyloid precursor protein (APP) (Tg-SwDI)). Cerebrovascular integrity was characterized by quantifying the occurrence of microinfarcts and haemorrhages and compared with wild-type mice without Aß. A significant increase in soluble Aß peptides (Aß40/42) was detected after 1 month of hypoperfusion in the parenchyma in parallel with elevated APP and APP proteolytic products. Following 3 months, a significant increase in insoluble Aß40/42 was determined in the parenchyma and vasculature. Microinfarct load was significantly increased in the Tg-SwDI as compared with wild-type mice and further exacerbated by hypoperfusion at 1 and 3 months. In addition, the number of Tg-SwDI hypoperfused mice with haemorrhages was increased compared with hypoperfused wild-type mice. Soluble parenchymal Aß was associated with elevated NADPH oxidase-2 (NOX2) which was exacerbated by 1-month hypoperfusion. We suggest that in response to hypoperfusion, increased Aß production/deposition may contribute to degenerative processes by triggering oxidative stress promoting cerebrovascular disruption and the development of microinfarcts.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/metabolismo
Isquemia Encefálica/complicações
Angiopatia Amiloide Cerebral/etiologia
Hemorragia Cerebral/etiologia
Infarto Cerebral/etiologia
Fragmentos de Peptídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Angiopatia Amiloide Cerebral/metabolismo
Angiopatia Amiloide Cerebral/patologia
Hemorragia Cerebral/metabolismo
Hemorragia Cerebral/patologia
Infarto Cerebral/metabolismo
Infarto Cerebral/patologia
Circulação Cerebrovascular/fisiologia
Doença Crônica
Modelos Animais de Doenças
Glicoproteínas de Membrana/metabolismo
Camundongos Transgênicos
NADPH Oxidase 2
NADPH Oxidases/metabolismo
Estresse Oxidativo/fisiologia
Tecido Parenquimatoso/metabolismo
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Membrane Glycoproteins); 0 (Peptide Fragments); 0 (amyloid beta-protein (40-42)); EC 1.6.3.- (Cybb protein, mouse); EC 1.6.3.- (NADPH Oxidase 2); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170962


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[PMID]:28476760
[Au] Autor:Pasi M; Boulouis G; Fotiadis P; Auriel E; Charidimou A; Haley K; Ayres A; Schwab KM; Goldstein JN; Rosand J; Viswanathan A; Pantoni L; Greenberg SM; Gurol ME
[Ad] Endereço:From the Hemorrhagic Stroke Research Program (M.P., G.B., P.F., E.A., A.C., K.H., A.A., K.M.S., A.V., S.M.G., M.E.G.), Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston; NEUROFARBA Department (M.P., L.P.), Neuroscience Section, University
[Ti] Título:Distribution of lacunes in cerebral amyloid angiopathy and hypertensive small vessel disease.
[So] Source:Neurology;88(23):2162-2168, 2017 Jun 06.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate whether the burden of deep and lobar lacunes differs between patients with intracerebral hemorrhage (ICH) with definite/probable cerebral amyloid angiopathy (CAA) per the Boston criteria and hypertensive small vessel disease (HTN-SVD; ICH in basal ganglia, thalami, brainstem). METHODS: We defined lobar and deep lacunes similar to the topographic distribution used for ICH and cerebral microbleeds (CMBs). We then compared their distribution between patients with CAA-ICH and those with strictly deep CMB and ICH (HTN-ICH). The independent associations of lacune location with the diagnosis of CAA-ICH and HTN-ICH were evaluated with multivariable models. The relationship between lobar lacunes and white matter hyperintensity (WMH) volume was evaluated by means of partial correlation analyses adjusted for age and a validated visual scale. RESULTS: In our final cohort of 316 patients with ICH, lacunes were frequent (24.7%), with similar rates in 191 patients with CAA and 125 with HTN-ICH (23% vs 27.2%, = 0.4). Lobar lacunes were more commonly present in CAA (20.4% vs 5.7%, < 0.001), while deep lacunes were more frequent in HTN-ICH (15.2% vs 2.1%, < 0.001). After correction for demographics and clinical and neuroimaging markers of SVD, lobar lacunes were associated with CAA ( = 0.003) and deep lacunes with HTN-ICH ( < 0.001). Lobar lacunes in 80% of the cases were at least in contact with WMH, and after adjustment for age, they were highly correlated to WMH volume ( = 0.42, < 0.001). CONCLUSIONS: Lobar lacunes are associated with CAA, whereas deep lacunes are more frequent in HTN-SVD. Lobar lacunes seem to have a close relationship with WMH, suggesting a possible common origin.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Angiopatia Amiloide Cerebral/diagnóstico por imagem
Hemorragia Cerebral/diagnóstico por imagem
Doenças de Pequenos Vasos Cerebrais/diagnóstico por imagem
Hipertensão/diagnóstico por imagem
Acidente Vascular Cerebral/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Boston
Angiopatia Amiloide Cerebral/complicações
Angiografia Cerebral
Hemorragia Cerebral/complicações
Doenças de Pequenos Vasos Cerebrais/complicações
Angiografia por Tomografia Computadorizada
Feminino
Seres Humanos
Hipertensão/complicações
Modelos Logísticos
Imagem por Ressonância Magnética
Masculino
Análise Multivariada
Estudos Prospectivos
Acidente Vascular Cerebral/complicações
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004007



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