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Cerebral amyloid angiopathy

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https://www.readbyqxmd.com/read/28801214/lobar-hemorrhage-induced-by-acquired-factor-xiii-deficiency-in-a-patient-with-cerebral-amyloid-angiopathy
#1
Hidetaka Arishima, Hiroyuki Neishi, Ken-Ichiro Kikuta, Mihoko Morita, Naoko Hosono, Takahiro Yamauchi, Masayoshi Souri, Akitada Ichinose
A 68-year-old man presented with intracranial hemorrhage in the right frontal lobe, which rapidly increased the day after admission. We performed hematoma removal with a biopsy of the cortex around the hematoma. The day after the operation, a subcutaneous hematoma over the craniotomy appeared, and the computed tomography showed a recurrent hemorrhage with an acute subdural hematoma. We were aware of a bleeding tendency, and a detailed hematologic examination by hematologists revealed autoimmune acquired factor XIII deficiency due to an antifactor XIII antibody...
August 8, 2017: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
https://www.readbyqxmd.com/read/28761931/unc5c-variants-are-associated-with-cerebral-amyloid-angiopathy
#2
Hyun-Sik Yang, Charles C White, Lori B Chibnik, Hans-Ulrich Klein, Julie A Schneider, David A Bennett, Philip L De Jager
OBJECTIVE: To determine whether common genetic variants in UNC5C, a recently identified late-onset Alzheimer disease (LOAD) dementia susceptibility gene, are associated with AD susceptibility or AD-related clinical/pathologic phenotypes. METHODS: We used data from deceased individuals of European descent who participated in the Religious Orders Study or the Rush Memory and Aging Project (n = 1,288). We examined whether there were associations between single nucleotide polymorphisms (SNPs) within ±100 kb of the UNC5C gene and a diagnosis of AD dementia, global cognitive decline, a pathologic diagnosis of AD, β-amyloid load, neuritic plaque count, diffuse plaque count, paired helical filament tau density, neurofibrillary tangle count, and cerebral amyloid angiopathy (CAA) score...
August 2017: Neurology. Genetics
https://www.readbyqxmd.com/read/28760945/inactivation-of-nitric-oxide-synthesis-exacerbates-the-development-of-alzheimer-disease-pathology-in-appps1-mice-amyloid-precursor-protein-presenilin-1
#3
Diana Cifuentes, Marine Poittevin, Philippe Bonnin, Anta Ngkelo, Nathalie Kubis, Tatyana Merkulova-Rainon, Bernard I Lévy
The epidemiological link between hypertension and Alzheimer disease is established. We previously reported that hypertension aggravates the Alzheimer-like pathology in APPPS1 mice (amyloid precursor protein/presenilin-1, mouse model of Alzheimer disease) with angiotensin II-induced hypertension, in relation with hypertension and nitric oxide deficiency. To provide further insights into the role of nitric oxide in the hypertension-Alzheimer disease cross-talk, we studied the effects of nitric oxide blockade in APPPS1 mice using N(ω)-nitro-l-arginine methyl ester (l-NAME) alone or in combination with hydralazine, to normalize blood pressure...
July 31, 2017: Hypertension
https://www.readbyqxmd.com/read/28757406/subdural-hemorrhage-from-cerebral-amyloid-angiopathy-related-intracerebral-hemorrhage-a-risk-factor-for-postoperative-hemorrhage
#4
Lei Xia, Wen Min, Xianghe Lu, Chengde Wang, Zeping Jiang, Yu Zhang, Sheng Ye, Zhipeng Su, Weiming Zheng, Meihao Wang, Jianmin Li, Jinseng Wu, Qichuan Zhuge
OBJECTIVE: Surgical treatment for cerebral amyloid angiopathy (CAA)-related intracerebral hemorrhage (ICH) remains controversial. A subset of CAA-related ICH with associated subdural hemorrhage (SDH), has been reported. This study aimed to evaluate the clinical results and surgical outcomes of this type of ICH with associated SDH. METHODS: Ninety-eight cases of CAA-related ICH who met Boston criteria, were enrolled in the study. They were divided into those with and without SDH...
July 27, 2017: World Neurosurgery
https://www.readbyqxmd.com/read/28747441/brain-hemorrhage-recurrence-small-vessel-disease-type-and-cerebral-microbleeds-a-meta-analysis
#5
Andreas Charidimou, Toshio Imaizumi, Solene Moulin, Alexandro Biffi, Neshika Samarasekera, Yusuke Yakushiji, Andre Peeters, Yves Vandermeeren, Patrice Laloux, Jean-Claude Baron, Mar Hernandez-Guillamon, Joan Montaner, Barbara Casolla, Simone M Gregoire, Dong-Wha Kang, Jong S Kim, H Naka, Eric E Smith, Anand Viswanathan, Hans R Jäger, Rustam Al-Shahi Salman, Steven M Greenberg, Charlotte Cordonnier, David J Werring
OBJECTIVE: We evaluated recurrent intracerebral hemorrhage (ICH) risk in ICH survivors, stratified by the presence, distribution, and number of cerebral microbleeds (CMBs) on MRI (i.e., the presumed causal underlying small vessel disease and its severity). METHODS: This was a meta-analysis of prospective cohorts following ICH, with blood-sensitive brain MRI soon after ICH. We estimated annualized recurrent symptomatic ICH rates for each study and compared pooled odds ratios (ORs) of recurrent ICH by CMB presence/absence and presumed etiology based on CMB distribution (strictly lobar CMBs related to probable or possible cerebral amyloid angiopathy [CAA] vs non-CAA) and burden (1, 2-4, 5-10, and >10 CMBs), using random effects models...
July 26, 2017: Neurology
https://www.readbyqxmd.com/read/28734389/inflammatory-variant-of-cerebral-amyloid-angiopathy
#6
M A Espinoza Marcos, A López-Rueda
No abstract text is available yet for this article.
July 19, 2017: Radiología
https://www.readbyqxmd.com/read/28731431/association-between-cholesterol-exposure-and-neuropathological-findings-the-act-study
#7
Brianne M Bettcher, M Colin Ard, Bruce R Reed, Andreana Benitez, Amanda Simmons, Eric B Larson, Josh A Sonnen, Thomas J Montine, Ge Li, C Dirk Keene, Paul K Crane, Dan Mungas
We characterized the relationship between late life cholesterol exposure and neuropathological outcomes in a community-based, older adult cohort. Adult Changes in Thought (ACT) is a cohort study that enrolls consenting, randomly selected, non-demented people aged ≥65 from a healthcare delivery system. We used late life HDL and total cholesterol lab values from Group Health computerized records, and calculated HDL and non-HDL levels. We evaluated neuropathological outcomes of Alzheimer's disease, cerebral amyloid angiopathy, vascular brain injury, and Lewy body disease...
July 19, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28724587/florbetapir-imaging-in-cerebral-amyloid-angiopathy-related-hemorrhages
#8
Nicolas Raposo, Mélanie Planton, Patrice Péran, Pierre Payoux, Fabrice Bonneville, Aicha Lyoubi, Jean François Albucher, Blandine Acket, Anne Sophie Salabert, Jean Marc Olivot, Anne Hitzel, François Chollet, Jérémie Pariente
OBJECTIVE: To assess whether (18)F-florbetapir, a PET amyloid tracer, could bind vascular amyloid in cerebral amyloid angiopathy (CAA) by comparing cortical florbetapir retention during the acute phase between patients with CAA-related lobar intracerebral hemorrhage (ICH) and patients with hypertension-related deep ICH. METHODS: Patients with acute CAA-related lobar ICH were prospectively enrolled and compared with patients with deep ICH. (18)F-florbetapir PET, brain MRI, and APOE genotype were obtained for all participants...
July 19, 2017: Neurology
https://www.readbyqxmd.com/read/28720659/microbleeds-cerebral-hemorrhage-and-functional-outcome-after-stroke-thrombolysis-individual-patient-data-meta-analysis
#9
Andreas Charidimou, Guillaume Turc, Catherine Oppenheim, Shenqiang Yan, Jan F Scheitz, Hebun Erdur, Pascal P Klinger-Gratz, Marwan El-Koussy, Wakoh Takahashi, Yusuke Moriya, Duncan Wilson, Chelsea S Kidwell, Jeffrey L Saver, Asma Sallem, Solene Moulin, Myriam Edjlali-Goujon, Vincent Thijs, Zoe Fox, Ashkan Shoamanesh, Gregory W Albers, Heinrich P Mattle, Oscar R Benavente, H Rolf Jäger, Gareth Ambler, Junya Aoki, Jean-Claude Baron, Kazumi Kimura, Wataru Kakuda, Shunya Takizawa, Simon Jung, Christian H Nolte, Min Lou, Charlotte Cordonnier, David J Werring
BACKGROUND AND PURPOSE: We assessed whether the presence, number, and distribution of cerebral microbleeds (CMBs) on pre-intravenous thrombolysis MRI scans of acute ischemic stroke patients are associated with an increased risk of intracerebral hemorrhage (ICH) or poor functional outcome. METHODS: We performed an individual patient data meta-analysis, including prospective and retrospective studies of acute ischemic stroke treated with intravenous tissue-type plasminogen activator...
July 18, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28717091/thrombolysis-related-multiple-lobar-hemorrhaging-in-cerebral-amyloid-angiopathy-with-extensive-strictly-lobar-cerebral-microbleeding
#10
Makoto Eriguchi, Yusuke Yakushiji, Jun Tanaka, Masashi Nishihara, Hideo Hara
A hemi-paralyzed 86-year-old man was diagnosed with ischemic stroke and underwent thrombolysis. Pre-thrombolysis brain magnetic resonance imaging revealed extensive strictly lobar cerebral microbleeding (CMB). Post-thrombolytic computed tomography revealed asymptomatic multiple intracerebral hemorrhaging (ICH). His age, CMB topography, and decreased cerebral spinal fluid amyloid-β 40 and 42 levels were compatible with a diagnosis of cerebral amyloid angiopathy (CAA). There is no consensus on the safety of thrombolysis for acute stroke patients with CAA...
2017: Internal Medicine
https://www.readbyqxmd.com/read/28707482/peripheral-inflammation-apolipoprotein-e4-and-amyloid-%C3%AE-interact-to-induce-cognitive-and-cerebrovascular-dysfunction
#11
Felecia M Marottoli, Yuriko Katsumata, Kevin P Koster, Riya Thomas, David W Fardo, Leon M Tai
Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer's disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. The goal of this study was to determine the interactive effect of APOE4, Aβ, and chronic repeated peripheral inflammation on cerebrovascular and cognitive dysfunction in vivo...
July 2017: ASN Neuro
https://www.readbyqxmd.com/read/28706123/cerebral-microbleeds-in-murine-amyloid-angiopathy-natural-course-and-anticoagulant-effects
#12
Marilena Marinescu, Li Sun, Marc Fatar, Andreas Neubauer, Lothar Schad, Joanne van Ryn, Lorenz Lehmann, Roland Veltkamp
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...
August 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28701379/loss-of-clusterin-shifts-amyloid-deposition-to-the-cerebrovasculature-via-disruption-of-perivascular-drainage-pathways
#13
Aleksandra M Wojtas, Silvia S Kang, Benjamin M Olley, Maureen Gatherer, Mitsuru Shinohara, Patricia A Lozano, Chia-Chen Liu, Aishe Kurti, Kelsey E Baker, Dennis W Dickson, Mei Yue, Leonard Petrucelli, Guojun Bu, Roxana O Carare, John D Fryer
Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) peptide deposition in brain parenchyma as plaques and in cerebral blood vessels as cerebral amyloid angiopathy (CAA). CAA deposition leads to several clinical complications, including intracerebral hemorrhage. The underlying molecular mechanisms that regulate plaque and CAA deposition in the vast majority of sporadic AD patients remain unclear. The clusterin (CLU) gene is genetically associated with AD and CLU has been shown to alter aggregation, toxicity, and blood-brain barrier transport of Aβ, suggesting it might play a key role in regulating the balance between Aβ deposition and clearance in both brain and blood vessels...
August 15, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28700676/imaging-features-of-intracerebral-hemorrhage-with-cerebral-amyloid-angiopathy-systematic-review-and-meta-analysis
#14
Neshika Samarasekera, Mark Alexander Rodrigues, Pheng Shiew Toh, Rustam Al-Shahi Salman
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")...
2017: PloS One
https://www.readbyqxmd.com/read/28697558/comparative-analysis-of-cortical-microinfarcts-and-microbleeds-using-3-0-tesla-postmortem-magnetic-resonance-images-and-histopathology
#15
Atsushi Niwa, Yuichiro Ii, Akihiro Shindo, Ko Matsuo, Hidehiro Ishikawa, Akira Taniguchi, Shinichi Takase, Masayuki Maeda, Hajime Sakuma, Hiroyasu Akatsu, Yoshio Hashizume, Hidekazu Tomimoto
Microvascular lesions including cortical microinfarctions (CMIs) and cerebral lobar microbleeds (CMBs) are usually caused by cerebral amyloid angiopathy (CAA) in the elderly and are correlated with cognitive decline. However, their radiological-histopathological coincidence has not been revealed systematically with widely used 3-Tesla (3T) magnetic resonance imaging (MRI). The purpose of the present study is to delineate the histopathological background corresponding to MR images of these lesions. We examined formalin-fixed 10-mm thick coronal brain blocks from 10 CAA patients (five were also diagnosed with Alzheimer's disease, three with dementia with Lewy bodies, and two with CAA only) with dementia and six non CAA patients with neurodegenerative disease...
2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28677558/cerebral-amyloid-angiopathy-and-implications-for-atrial-fibrillation-management
#16
Christopher V DeSimone, Jonathan Graff-Radford, Majd A El-Harasis, Alejandro A Rabinstein, Samuel J Asirvatham, David R Holmes
No abstract text is available yet for this article.
July 1, 2017: Lancet
https://www.readbyqxmd.com/read/28677497/platelets-their-potential-contribution-to-the-generation-of-beta-amyloid-plaques-in-alzheimer-s-disease
#17
Christian Humpel
BACKGROUND: Alzheimer's disease is a severe neurodegenerative brain disorder, showing severe beta-amyloid depositions in the brain (plaques) and in vessels (cerebral amyloid angiopathy, CAA), tau pathology, neurodegeneration (and loss of acetylcholine), inflammation with reactive astrocytes and microglia and cerebrovascular damage, all resulting in memory loss. METHODS AND RESULTS: In this review I present a hypothesis that chronic vascular lesions and bleedings cause platelet overactivation and repair...
July 5, 2017: Current Neurovascular Research
https://www.readbyqxmd.com/read/28670089/usefulness-of-positron-emission-tomography-to-detect-cerebral-amyloid-as-a-means-to-diagnose-neurodegenerative-disease
#18
Jessica Page, Umesh Oza, Kennith Layton, Claudia Padilla
Alzheimer's disease is characterized histologically by the accumulation of a subtype of amyloid protein-beta amyloid-in the brain parenchyma in the form of amyloid plaques. In another neurodegenerative disorder, cerebral amyloid angiopathy, the accumulation of beta amyloid occurs within the walls of the cerebral vessels. With recent advances in imaging technology, we can not only image amyloid plaques in the brain parenchyma at an earlier stage of disease, but can also often correlate the presence of Alzheimer's disease with cerebral amyloid angiopathy...
July 2017: Proceedings of the Baylor University Medical Center
https://www.readbyqxmd.com/read/28667120/chronic-cerebral-hypoperfusion-alters-amyloid-%C3%AE-peptide-pools-leading-to-cerebral-amyloid-angiopathy-microinfarcts-and-hemorrhages-in-tg-swdi-mice
#19
Natalia Salvadores, James L Searcy, Philip R Holland, Karen Horsburgh
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 hypothesised that cerebral hypoperfusion promotes the accumulation of amyloid-β (Ab) 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 Ab peptide pools in a transgenic mouse model of AD (Tg-SwDI) at an age when fibrillar amyloid burden is minimal...
June 30, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28647708/relapsing-cerebral-amyloid-angiopathy-related-inflammation-the-wax-and-the-wane
#20
Sharfaraz Salam, Mayooreshan Anandarajah, Sarah Al-Bachari, Piyali Pal, Jonathan Sussman, Hisham Hamdalla
Cerebral amyloid angiopathy-related inflammation (CAA-I) is a rare variant of cerebral amyloid angiopathy (CAA). Its precise pathophysiology remains uncertain and we currently have limited evidence on which immunosuppressive agents are the most effective in its treatment. The disease course of CAA-I disorders can vary from an isolated clinical event to recurrent episodes. We present a case of biopsy-confirmed CAA-I that gives insight into its potential relapsing nature and the challenges of its long-term management...
June 24, 2017: Practical Neurology
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