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Journal articles on the topic 'CAA'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Babu, Numbury Surendra, and Didugu Jayaprakash. "Computational Study of the Stability of Tautomers and equilibrium constants of Cyanuric acid (CA) in Different solvents." JOURNAL OF ADVANCES IN CHEMISTRY 11, no. 2 (2015): 3485–97. http://dx.doi.org/10.24297/jac.v11i2.6691.

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In the present investigation, the tautomeric and equilibrium of Cyanuric acid has been studied using Hartifock (HF) method in the gas phase and different solvents using the PCM model. The relative energies of these tautomers have been calculated at the HF level of theory using 6-311++ G (d,p) basis set. Energetics and relative stabilities of the tautomers were compared and analyzed in both the gaseous and different solvents. The results indicate that the keto tautomer (CA1) is the most stable form in the gas phase and other solvents. The order of stability of isomers was found to be CA1 > C

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Ali, Nur Shidaa Mohd, Abu Bakar Salleh, Thean Chor Leow, Raja Noor Zaliha Raja Abd Rahman, and Mohd Shukuri Mohamad Ali. "The Influence of Calcium toward Order/Disorder Conformation of Repeat-in-Toxin (RTX) Structure of Family I.3 Lipase from Pseudomonas fluorescens AMS8." Toxins 12, no. 9 (2020): 579. http://dx.doi.org/10.3390/toxins12090579.

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Calcium-binding plays a decisive role in the folding and stabilization of many RTX proteins, especially for the RTX domain. Although many studies have been conducted to prove the contribution of Ca2+ ion toward the folding and stabilization of RTX proteins, its functional dynamics and conformational structural changes remain elusive. Here, molecular docking and molecular dynamics (MD) simulations were performed to analyze the contribution of Ca2+ ion toward the folding and stabilization of the RTX lipase (AMS8 lipase) structure. AMS8 lipase contains six Ca2+ ions (Ca1–Ca6). Three Ca2+ ions (Ca

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Van Binh, Le, and Ngo Thi Thu Thao. "Effects of Calcium Levels in Artificial Pellet Feed on the Growth and Survival Rate of Black Apple Snails (Pila polita)." Vietnam Journal of Agricultural Sciences 2, no. 2 (2019): 387–96. http://dx.doi.org/10.31817/vjas.2019.2.2.04.

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The present study was conducted to evaluate the effects of different dietary calcium levels on the growth and survival rate of black apple snails (Pila polita) in the grow-out period. There were 3 replicates for each treatment and the snails were fed with five calcium levels (% dry matter) in diet as follows: 1% (Ca1), 3% (Ca3), 5% (Ca5), 7% (Ca7), and 9% (Ca9). Two-month-old juveniles with an average initial body weight of 2.13g, shell height of 21.71mm, and shell width of 16.35mm were reared in tarpaulin tanks (1 × 1 × 1m; 40cm water depth) at the density of 100 individuals per tank. After 4

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Cai, Shixuan, Hongyan Shi, Guoqian Li, et al. "3D-Printed Concentration-Controlled Microfluidic Chip with Diffusion Mixing Pattern for the Synthesis of Alginate Drug Delivery Microgels." Nanomaterials 9, no. 10 (2019): 1451. http://dx.doi.org/10.3390/nano9101451.

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Alginate as a good drug delivery vehicle has excellent biocompatibility and biodegradability. In the ionic gelation process between alginate and Ca2+, the violent reaction is the absence of a well-controlled strategy in the synthesizing calcium alginate (CaA) microgels. In this study, a concentration-controlled microfluidic chip with central buffer flow was designed and 3D-printed to well-control the synthesis process of CaA microgels by the diffusion mixing pattern. The diffusion mixing pattern in the microfluidic chip can slow down the ionic gelation process in the central stream. The partic

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Mayo, Sherry. "CAA 2011." Visual Inquiry 1, no. 1 (2011): 89–92. http://dx.doi.org/10.1386/vi.1.1.89_4.

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6

Kirsch, Tess. "CAA Updates." Perspectives on Issues in Higher Education 6, no. 2 (2003): 10. http://dx.doi.org/10.1044/ihe6.2.10.

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Renard, Dimitri, Birama Sangare, Ansma Youssouf, and Eric Thouvenot. "Intracranial Drain-Related Intracerebral Hemorrhage in Two Sporadic Cerebral Amyloid Angiopathy Patients." Journal of Alzheimer's Disease Reports 8, no. 1 (2024): 1089–92. http://dx.doi.org/10.3233/adr-240086.

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Alzheimer’s disease and cerebral amyloid angiopathy (CAA) are often associated. Amyloid accumulation within leptomeningeal and small/median-sized cerebral blood vessels in CAA results in vessel fragility, leading to spontaneous leptomeningeal bleeding, lobar intracerebral hemorrhage (ICH) and cerebral microbleeds. CAA is also associated with non-traumatic subdural hematoma. The role of CAA-related vessel fragility in hemorrhagic complications after trauma, brain surgery, and intracranial drain insertion in CAA is unknown. We present two sporadic CAA patients with intracranial drain-related ICH

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8

Han, Byung Hee, Meng-liang Zhou, Andrew W. Johnson, et al. "Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice." Proceedings of the National Academy of Sciences 112, no. 8 (2015): E881—E890. http://dx.doi.org/10.1073/pnas.1414930112.

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Cerebral amyloid angiopathy (CAA) is characterized by deposition of amyloid β peptide (Aβ) within walls of cerebral arteries and is an important cause of intracerebral hemorrhage, ischemic stroke, and cognitive dysfunction in elderly patients with and without Alzheimer’s Disease (AD). NADPH oxidase-derived oxidative stress plays a key role in soluble Aβ-induced vessel dysfunction, but the mechanisms by which insoluble Aβ in the form of CAA causes cerebrovascular (CV) dysfunction are not clear. Here, we demonstrate evidence that reactive oxygen species (ROS) and, in particular, NADPH oxidase-de

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9

KASE, Kiwamu. "An Introduction of Outline of CAD/CAE/CAM/CAT (1)." Journal of the Japan Society for Precision Engineering 79, no. 2 (2013): 144–47. http://dx.doi.org/10.2493/jjspe.79.144.

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KASE, Kiwamu. "An Introduction of Outline of CAD/CAE/CAM/CAT (2)." Journal of the Japan Society for Precision Engineering 79, no. 3 (2013): 223–26. http://dx.doi.org/10.2493/jjspe.79.223.

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KASE, Kiwamu. "An Introduction of Outline of CAD/CAE/CAM/CAT (3)." Journal of the Japan Society for Precision Engineering 79, no. 4 (2013): 309–13. http://dx.doi.org/10.2493/jjspe.79.309.

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12

Rasing, Ingeborg, Sabine Voigt, Emma A. Koemans, et al. "Occipital Cortical Calcifications in Cerebral Amyloid Angiopathy." Stroke 52, no. 5 (2021): 1851–55. http://dx.doi.org/10.1161/strokeaha.120.033286.

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Background and Purpose: Cortical calcifications have been reported in patients with cerebral amyloid angiopathy (CAA), although their prevalence and pathophysiology are unknown. We investigated the frequency of calcifications on computed tomography, their association with intracerebral hemorrhage (ICH) and their coexistence with a striped pattern of the occipital cortex reflecting microcalcifications on ultra-high-field 7T-magnetic resonance imaging in Dutch-type hereditary CAA (D-CAA) and sporadic CAA. Methods: We included D-CAA mutation carriers with a proven APP (amyloid precursor protein)

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Guidoux, Celine, Jean-Jacques Hauw, Isabelle F. Klein, et al. "Amyloid Angiopathy in Brain Hemorrhage: A Postmortem Neuropathological-Magnetic Resonance Imaging Study." Cerebrovascular Diseases 45, no. 3-4 (2018): 124–31. http://dx.doi.org/10.1159/000486554.

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Background: Risk factors for intracerebral hemorrhage (ICH) include hypertension and cerebral amyloid angiopathy (CAA). The objective of this study was to determine the autopsy prevalence of CAA and the potential overlap with other risk factors among patients who died from ICH and also the correlation of CAA with cerebral microbleeds. Methods: We analyzed 81 consecutive autopsy brains from patients with ICH. Staining for CAA detection was performed. We used an age- and sex-matched control group of routine brain autopsies of nonneurological patients to determine the frequencies of CAA and hyper

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Hoffman-Zacharska, Dorota, and Anna Sulek. "The New Face of Dynamic Mutation—the CAA [CAG]n CAA CAG Motif as a Mutable Unit in the TBP Gene Causative for Spino-Cerebellar Ataxia Type 17." International Journal of Molecular Sciences 25, no. 15 (2024): 8190. http://dx.doi.org/10.3390/ijms25158190.

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Since 1991, several genetic disorders caused by unstable trinucleotide repeats (TNRs) have been identified, collectively referred to as triplet repeat diseases (TREDs). They share a common mutation mechanism: the expansion of repeats (dynamic mutations) due to the propensity of repeated sequences to form unusual DNA structures during replication. TREDs are characterized as neurodegenerative diseases or complex syndromes with significant neurological components. Spinocerebellar ataxia type 17 (SCA17) falls into the former category and is caused by the expansion of mixed CAA/CAG repeats in the T

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15

Agnew, A., A. J. C. Fulford, N. De Jonge, et al. "The relationship between worm burden and levels of a circulating antigen (CAA) of five species of Schistosoma in mice." Parasitology 111, no. 1 (1995): 67–76. http://dx.doi.org/10.1017/s0031182000064611.

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SUMMARYThis study examines the ability of an assay which measures the amount of a schistosome specific antigen (CAA) in the host circulation to reliably reflect relative worm burden. Mice were infected with 5 species of schistosome with a range of infection dose. The levels of serum CAA increased during schistosome maturation. In all species tested CAA levels correlated well with adult worm burden once the parasites achieved sexual maturity and remained relatively stable during the establishment of egg production. The amount of CAA produced varied between species but within each species CAA le

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Graff-Radford, Jonathan, Timothy G. Lesnick, Michelle M. Mielke, et al. "Cerebral Amyloid Angiopathy Burden and Cerebral Microbleeds: Pathological Evidence for Distinct Phenotypes." Journal of Alzheimer's Disease 81, no. 1 (2021): 113–22. http://dx.doi.org/10.3233/jad-201536.

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Background: The relationship between cerebral microbleeds (CMBs) on hemosiderin-sensitive MRI sequences and cerebral amyloid angiopathy (CAA) remains unclear in population-based participants or in individuals with dementia. Objective: To determine whether CMBs on antemortem MRI correlate with CAA. Methods: We reviewed 54 consecutive participants with antemortem T2*GRE-MRI sequences and subsequent autopsy. CMBs were quantified on MRIs closest to death. Autopsy CAA burden was quantified in each region including leptomeningeal/cortical and capillary CAA. By a clustering approach, we examined the

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JIN, CHUNBO, BOYAN MAO, BAO LI, et al. "HEMODYNAMIC STUDY OF CORONARY ARTERY ANEURYSMS." Journal of Mechanics in Medicine and Biology 20, no. 03 (2020): 2050012. http://dx.doi.org/10.1142/s0219519420500128.

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Background: When the coronary artery expands more than two times its diameter, it will form a coronary artery aneurysm (CAA). CAA can lead to myocardial ischemia. In this paper, the mechanism of myocardial ischemia induced by CAA was studied by geometric multiscale method. Methods: Four kinds of three-dimensional models of CAA with different dilation diameters were established on the basis of normal three-dimensional models. The dilation diameters were 2, 3, 5 and 7 times, capacitance was added after the CAA to simulate the elasticity of the vascular wall. Results:A large number of eddies exis

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18

Tsai, Hsin-Hsi, Marco Pasi, Li-Kai Tsai, et al. "Centrum Semiovale Perivascular Space and Amyloid Deposition in Spontaneous Intracerebral Hemorrhage." Stroke 52, no. 7 (2021): 2356–62. http://dx.doi.org/10.1161/strokeaha.120.032139.

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Background and Purpose: We explored whether high-degree magnetic resonance imaging–visible perivascular spaces in centrum semiovale (CSO) are more prevalent in cerebral amyloid angiopathy (CAA) than hypertensive small vessel disease and their relationship to brain amyloid retention in patients with primary intracerebral hemorrhage (ICH). Methods: One hundred and eight spontaneous ICH patients who underwent magnetic resonance imaging and Pittsburgh compound B were enrolled. Topography and severity of enlarged perivascular spaces were compared between CAA-related ICH (CAA-ICH) and hypertensive s

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Jäkel, Lieke, William E. Van Nostrand, James A. R. Nicoll, David J. Werring, and Marcel M. Verbeek. "Animal models of cerebral amyloid angiopathy." Clinical Science 131, no. 19 (2017): 2469–88. http://dx.doi.org/10.1042/cs20170033.

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Cerebral amyloid angiopathy (CAA), due to vascular amyloid β (Aβ) 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 ar

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20

Kulesh, A. A., N. Kh Gorst, V. E. Drobakha, N. A. Kaileva, and V. V. Shestakov. "Cortical superficial siderosis is a new MRT-phenomenon in neurological practice: clinical observations and review of literature." Perm Medical Journal 35, no. 5 (2018): 82–92. http://dx.doi.org/10.17816/pmj35582-92.

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Cerebral amyloid angiopathy (CAA) is a specific variant of cerebral small vessel disease, associated with high risk of spontaneous intracerebral bleedings, cognitive disorders and hemorrhagic complications of antithrombotic and thrombolytic therapy. One of key markers of CAA is a relatively rare neurovisual phenomenon – cortical superficial siderosis (CSS). Two clinical cases of CAA with CSS are described in the present paper. In the first case, typical CAA complication were observed: intracerebral bleeding and cognitive disorders. In the second case, CAA was symptom-free. Analysis of clinical

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Barbato, Carmen, Piergiuseppe Liuzzi, Anna Maria Romoli, et al. "The Impact of Cerebral Amyloid Angiopathy on Functional Outcome of Patients Affected by Spontaneous Intracerebral Hemorrhage Discharged from Intensive Inpatient Rehabilitation: A Cohort Study." Diagnostics 12, no. 10 (2022): 2458. http://dx.doi.org/10.3390/diagnostics12102458.

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Background: Sporadic CAA is recognized as a major cause of sICH and sABI. Even if intensive rehabilitation is recommended to maximize functional recovery after sICH, no data are available on whether CAA may affect rehabilitation outcomes. In this observational prospective study, to explore the impact of CAA on rehabilitation results, functional outcomes after intensive rehabilitation have been compared between patients affected by sICH with and without a diagnosis of CAA. Methods: All adults affected by sABI due to sICH and admitted to the IRU of IRCCS-Don-Gnocchi-Foundation were consecutively

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Matsuda, Kana, Akihiro Shindo, Yuichiro Ii, et al. "Investigation of hypertensive arteriopathy-related and cerebral amyloid angiopathy-related small vessel disease scores in patients from a memory clinic: a prospective single-centre study." BMJ Open 11, no. 4 (2021): e042550. http://dx.doi.org/10.1136/bmjopen-2020-042550.

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ObjectiveThe severity of cerebral small vessel disease (SVD) is assessed through neuroimaging findings, including hypertensive arteriopathy (HA)-SVD and cerebral amyloid angiopathy (CAA)-SVD. HA-SVD and CAA-SVD have been collectively estimated as total scores: the HA-SVD and CAA-SVD scores, respectively. Previous reports suggest that HA-SVD scores are associated with cognitive function; however, the relationship between CAA-SVD scores and cognitive function remains unclear. Therefore, we examined the association between CAA-SVD scores and cognitive function. Furthermore, we developed a modifie

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De Reuck, Jacques. "The Impact of Cerebral Amyloid Angiopathy in Various Neurodegenerative Dementia Syndromes: A Neuropathological Study." Neurology Research International 2019 (January 16, 2019): 1–5. http://dx.doi.org/10.1155/2019/7247325.

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Purpose. The Boston criteria for cerebral amyloid angiopathy (CAA) have to be confirmed by postmortem examination. The present study investigates the incidence and the cerebrovascular impact of the severity of CAA in various neurodegenerative dementia diseases.Material and Methods. 208 patients underwent an autopsy. They consisted of 92 brains with Alzheimer’s disease (AD), 46 with frontotemporal lobar degeneration (FTLD), 24 with progressive supranuclear palsy (PSP), 21 with Lewy body dementia (LBD), 5 with corticobasal degeneration (CBD), and 20 controls. In addition to the macroscopic exami

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Kwan, Marilyn L., Noel Pimentel, Monika Izano, et al. "Adherence to cardiovascular medications and risk of cardiovascular disease in breast cancer patients: A causal inference approach in the Pathways Heart Study." PLOS ONE 19, no. 9 (2024): e0310531. http://dx.doi.org/10.1371/journal.pone.0310531.

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Purpose Women with breast cancer (BC) are at high risk of developing cardiovascular disease (CVD). We examined adherence to CVD medications and their association with major CVD events over 14 years of follow-up in the Pathways Heart Study, a prospective study of 4,776 stage I-III BC patients diagnosed from 2005–2013. Methods Eligibility included being alive 6 months post-BC diagnosis, with dyslipidemia, hypertension, or diabetes at diagnosis along with ≥1 prior outpatient order or dispensing for a statin, anti-hypertensive, or diabetes medication, respectively, in the 30 months prior. Medicati

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Li, Huadong, Hong Yu, Yu Song, et al. "Successful Surgical Treatment of a Giant Left Coronary Artery Aneurysm with Fistula." Heart Surgery Forum 24, no. 5 (2021): E868—E869. http://dx.doi.org/10.1532/hsf.3877.

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Coronary artery aneurysm (CAA) is an aortic catastrophe with low prevalence. Giant CAA is even more uncommon, requiring surgical intervention. Giant CAA usually originates from the proximal segments of the right coronary and the anterior descending arteries. Here we report a rare case of giant left CAA with fistula formation treated with successful surgery.

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Jiang, Danye, Shivi Garg, Romeesa Khan, and Louise McCullough. "Abstract WP380: Oligodendrocytes Damage in Cerebral Amyloid Angiopathy." Stroke 56, Suppl_1 (2025). https://doi.org/10.1161/str.56.suppl_1.wp380.

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Introduction: Cerebral amyloid angiopathy (CAA) leads to amyloid β (Aβ) deposition in the cortical and leptomeningeal vessels, and it is a largely untreatable cause of intracerebral hemorrhage and dementia. Studies estimate a 10-50% prevalence of CAA in the elderly population, positioning CAA as one of the strongest vascular contributors to age-related cognitive impairment. While reduced white matter (WM) volume and altered WM integrity have been reported in CAA, the response of oligodendrocytes – the specialized glial cells responsible for myelin production – to Aβ deposition remains unclear.

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SVEIKATA, Lukas, Maria Clara Zanon Zotin, Dorothee Schoemaker, et al. "Association of Blood Pressure Mean and Variability with Hippocampal Subfield Volumes in Cerebral Amyloid Angiopathy with Mild Cognitive Symptoms." Alzheimer's & Dementia 20, S2 (2024). https://doi.org/10.1002/alz.093298.

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AbstractBackgroundThe interaction between Alzheimer's pathology and cerebral amyloid angiopathy (CAA), a common cerebral small vessel disease, plays a crucial role in cognitive impairment development in older adults. Recent studies suggest that increased blood pressure (BP) variability may affect subclinical vascular disease and cognitive decline. However, it is currently unknown whether a particular BP profile is linked to hippocampal subfield volumes, which are a significant feature of cognitive decline in neurodegenerative diseases. Therefore, we conducted a study to investigate the relatio

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Araújo, Noemi S., Selvin Z. Reyes-Garcia, João A. F. Brogin, et al. "Chaotic and Stochastic Dynamics of Epileptiform-Like Activities in Sclerotic Hippocampus Resected from Patients with Pharmacoresistant Epilepsy." June 28, 2021. https://doi.org/10.5281/zenodo.5039479.

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This set contains 35 electrophysiological data recorded from slices of 12 human hippocampal specimens surgically resected from patients with pharmacoresistant temporal lobe epilepsy (TLE). The recordings were performed in the granule cell layer of the dentate gyrus (DG) and in the pyramidal cell layer of the CA1, CA2, CA3, CA4 and subiculum (SUB). The signals are organized in .txt files (which are easily importable), in terms of these hippocampal subfields and type of activity: interictal-like events (II) and periodic ictal spiking (PIS). The study was approved by the Ethics Committee of Unive

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Rahimov, Daler, Nayeem Nasher, Danial Ahmad, et al. "Management and Outcomes of Coronary Artery Aneurysms: A Patient-level Systematic Review." Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine, January 22, 2025. https://doi.org/10.1097/hpc.0000000000000381.

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Background: Data are lacking to guide standardized management of coronary artery aneurysms (CAA). We sought to analyze the available evidence in a quantitative manner. Methods: Electronic search identified 431 case reports or case series on CAA, comprising 488 patients. Patient-level data were extracted. Subgroups with (CAAF) and without fistulous connections (CAAO) were analyzed separately. Results: Fistulous connection was present in 24.0% (117/488) of patients with CAA. Angina was a presenting symptom in 64.7% (301/465), with higher preponderance in the CAAO group [CAAO: 71.1 % (249/350) vs

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Maramattom, Boby Varkey. "Cerebral Amyloid Angiopathy with Lobar Hemorrhages and CAA-Related Inflammation [CAA-RI] in an Indian Family." Cerebrovascular Diseases Extra, January 27, 2022. http://dx.doi.org/10.1159/000522214.

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Introduction; Cerebral amyloid angiopathy (CAA) is a common cause of lobar intracerebral hemorrhage [ICH]. Sporadic CAA is far more common than hereditary CAA [h-CAA]. Familial cerebral amyloid angiopathy has not yet been described from India. Case report; Two elderly Indian women (a mother and daughter) presented seven years apart with features of CAA. The mother had presented with features of CAA-related inflammation that responded to steroids, whereas the daughter presented with features of CAA-related intracerebral haemorrhage. Clinical exome testing did not reveal any known genetic varian

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Marola, Olivia J., Kristen D. Onos, Cory Diemler, Kelly J. Keezer, Michael Sasner, and Gareth R. Howell. "Identifying genetic risk factors driving cerebral amyloid angiopathy using novel mouse models." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.091446.

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AbstractBackgroundCerebral amyloid angiopathy (CAA) co‐occurs with neurodegeneration in Alzheimer’s disease (AD). CAA is absent in many AD mouse models, rendering CAA difficult to study. Previous work has shown wild‐derived WSB/EiJ (WSB) mice over‐expressing APP/PS1 had increased CAA, and thus may be useful in investigating CAA‐causing mechanisms. Here, genetic backgrounds with CAA susceptibility (WSB.APP/PS1) and resilience (B6.APP/PS1) are leveraged to map CAA‐susceptibility loci.Furthermore, blood brain barrier (BBB) compromise has been hypothesized to impair amyloid clearance and promote v

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Munsterman, Danielle, Sarina Falcione, Rebecca Long, et al. "Abstract WP242: Transcriptomic Changes In Peripheral Blood Leukocytes Associated With The Cerebral Amyloid Angiopathy Small Vessel Disease Score." Stroke 54, Suppl_1 (2023). http://dx.doi.org/10.1161/str.54.suppl_1.wp242.

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Introduction: Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease characterized by beta-amyloid deposition within cerebral vessels. Clinical markers of CAA severity include recurrent ICH, cognitive decline, and imaging features of CAA including microhemorrhage, dilated perivascular spaces, cortical superficial siderosis, and white matter hyperintensities. CAA is an important cause of cognitive decline and intracerebral hemorrhage in the elderly, leading to the need for CAA treatments. The contribution of the immune system to CAA severity is not well understood. This study sought to

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Dionne, Audrey, Anne Fournier, Ragui Ibrahim, Catherine Gebhard, and Nagib Dahdah. "Abstract 163: Regressed Coronary Aneurysm after Kawasaki Disease: What are they hiding? An Optical Coherence Tomography (OCT) study." Circulation 131, suppl_2 (2015). http://dx.doi.org/10.1161/circ.131.suppl_2.163.

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Background: Coronary artery aneurysms (CAA) are a serious complication of Kawasaki disease (KD). Regression of CAA occurs in 50% of the cases on follow up. Actual imaging techniques often described these segments as normal, whereas studies have shown significant endothelial and smooth muscle dysfunction. Method: KD patients scheduled for angiographic follow-up between June 2013 and August 2014 underwent OCT imaging. We compared coronary intimal changes in coronary artery segments with no history of CAA to segments with regressed CAA, and segments with persistent CAA. The intima was measured in

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"CAA chairman." Aircraft Engineering and Aerospace Technology 74, no. 1 (2002). http://dx.doi.org/10.1108/aeat.2002.12774aab.058.

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Jäkel, Lieke, Arno Stellingwerf, Anna M. Kort, et al. "Tissue inhibitor of matrix metalloproteinases 4: a novel marker associated with CAA." Alzheimer's & Dementia 19, S12 (2023). http://dx.doi.org/10.1002/alz.076737.

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AbstractBackgroundWe have previously shown that matrix metalloproteinase 9 (MMP9) and tissue inhibitor of proteinases 3 (TIMP3) are specifically expressed in the vasculature of patients with cerebral amyloid angiopathy (CAA). Moreover, we have demonstrated increased MMP9 and decreased TIMP3 levels, as well as an altered MMP9:TIMP3 ratio in the vasculature of CAA patients that suffered from intracerebral haemorrhages (CAA‐ICH) compared to CAA patients without ICH (CAA‐nonICH). We now extended our studies to investigate whether TIMP4 may have a similar role in CAA, as this has not been studied b

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Schrader, Joseph M., Feng Xu, Kevin J. Agostinucci, Nicholas A. DaSilva, and William E. Van Nostrand. "Longitudinal markers of cerebral amyloid angiopathy and related inflammation in rTg-DI rats." Scientific Reports 14, no. 1 (2024). http://dx.doi.org/10.1038/s41598-024-59013-7.

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AbstractCerebral amyloid angiopathy (CAA) is a prevalent vascular dementia and common comorbidity of Alzheimer’s disease (AD). While it is known that vascular fibrillar amyloid β (Aβ) deposits leads to vascular deterioration and can drive parenchymal CAA related inflammation (CAA-ri), underlying mechanisms of CAA pathology remain poorly understood. Here, we conducted brain regional proteomic analysis of early and late disease stages in the rTg-DI CAA rat model to gain molecular insight to mechanisms of CAA/CAA-ri progression and identify potential brain protein markers of CAA/CAA-ri. Longitudi

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Pyun, Jung‐Min, Min Ju Kang, Seung Jin Baek, Kyungbok Lee, Young Ho Park та SangYun Kim. "Magnetic resonance imaging‐negative cerebral amyloid angiopathy: cerebrospinal fluid amyloid‐β₄₂ over amyloid positron emission tomography". Alzheimer's & Dementia 20, S2 (2024). https://doi.org/10.1002/alz.087904.

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AbstractBackgroundCerebral amyloid angiopathy (CAA) pathology is becoming increasingly important in Alzheimer’s disease (AD) because of its potential link to amyloid‐related imaging abnormalities, a critical side effect observed during AD immunotherapy. Identification of CAA without typical magnetic resonance imaging (MRI) markers (MRI‐negative CAA) is challenging, and novel detection biomarkers are needed.MethodWe included 69 participants with high neuritic plaques (NP) burden, with and without CAA pathology (NP with CAA vs. NP without CAA) based on autopsy data from the Alzheimer’s Disease N

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Yin, Xiang‐Sha, Jianru Sun, Xue Wang, et al. "Prevalence of cerebral amyloid angiopathy and its correlation with Alzheimer's disease and cognition in an autopsy‐confirmed cohort from China." Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring 17, no. 2 (2025). https://doi.org/10.1002/dad2.70100.

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AbstractBACKGROUNDWe aimed to investigate the prevalence of cerebral amyloid angiopathy (CAA) and its correlations with Alzheimer's disease (AD) and cognitive impairment in an autopsy‐confirmed cohort donated to a human brain bank in Beijing, China.METHODSA total of 483 subjects were neuropathologically evaluated based on standardized protocols. Descriptive statistics and ordinal logistic regression models were used to estimate the correlation between CAA, AD, apolipoprotein E (APOE) genotyping, and cognitive function proximal to death.RESULTSNeuropathological assessment revealed that 53 of 48

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Handa, Takumi, Hayate Sasaki, Masaki Takao, Mitsutoshi Tano, and Yasuo Uchida. "Proteomics-based investigation of cerebrovascular molecular mechanisms in cerebral amyloid angiopathy by the FFPE-LMD-PCT-SWATH method." Fluids and Barriers of the CNS 19, no. 1 (2022). http://dx.doi.org/10.1186/s12987-022-00351-x.

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Abstract Background Cerebral amyloid angiopathy (CAA) occurs in 80% of patients with Alzheimer’s disease (AD) and is mainly caused by the abnormal deposition of Aβ in the walls of cerebral blood vessels. Cerebrovascular molecular mechanisms in CAA were investigated by using comprehensive and accurate quantitative proteomics. Methods Concerning the molecular mechanisms specific to CAA, formalin-fixed paraffin-embedded (FFPE) sections were prepared from patients having AD neuropathologic change (ADNC) with severe cortical Aβ vascular deposition (ADNC +/CAA +), and from patients having ADNC witho

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van den Berg, Emma, Johanna Nilsson, Iris Kersten, et al. "Cerebrospinal Fluid Panel of Synaptic Proteins in Cerebral Amyloid Angiopathy and Alzheimer’s Disease." Journal of Alzheimer's Disease, February 6, 2023, 1–9. http://dx.doi.org/10.3233/jad-220977.

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Background: Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) share pathogenic pathways related to amyloid-β deposition. Whereas AD is known to affect synaptic function, such an association for CAA remains yet unknown. Objective: We therefore aimed to investigate synaptic dysfunction in CAA. Methods: Multiple reaction monitoring mass spectrometry was used to quantify cerebrospinal fluid (CSF) concentrations of 15 synaptic proteins in CAA and AD patients, and age- and sex-matched cognitively unimpaired controls. Results: We included 25 patients with CAA, 49 patients with AD, and 25

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Martinez-Ramirez, Sergi, Jose-Rafael Romero, M. Edip Gurol, et al. "Abstract W P246: Diagnostic Value of Lobar Hemorrhages for Cerebral Amyloid Angiopathy in Hospital and Community-based Individuals: A Pathological Correlation Study." Stroke 45, suppl_1 (2014). http://dx.doi.org/10.1161/str.45.suppl_1.wp246.

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Objectives: To determine and compare the accuracy of the Boston criteria for the diagnosis of cerebral amyloid angiopathy (CAA) applied to: 1) a large hospital-based cohort; 2) a cohort of community-dwelling individuals. Methods: Among patients seen at a single academic medical center and participants enrolled in the Framingham Heart Study (FHS) we identified all individuals having had brain MRI (including hemosiderin-specific sequences) and pathological assessment of CAA at age ≥55. CAA was defined as Vonsattel degree ≥2, except in non-autopsy studies, where any vascular amloyid deposition wa

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Hondius, David, Robert Veerhuis, Ka Wan Li, et al. "Full complement activation is associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease." Alzheimer's & Dementia 19, S12 (2023). http://dx.doi.org/10.1002/alz.076151.

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AbstractBackgroundAlzheimer’s disease is the most common form of dementia and mainly characterized by the accumulation the amyloid β (Aβ) peptide in the parenchyma and often around the blood vessels of the brain. The accumulation of Aβ in vessels walls is referred to as cerebral amyloid angiopathy (CAA). In a subset of AD cases CAA is observed in both capillaries and larger vessels which is designated as CAA type‐1. CAA type‐1 is associated with an increased neuroinflammatory response involving activated microglia and increased oxidative stress, which supposedly results in loss of blood‐brain

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Storti, Benedetta, Maria Magdalena Gabriel, Stefan Sennfält, et al. "Rare forms of cerebral amyloid angiopathy: pathogenesis, biological and clinical features of CAA-ri and iCAA." Frontiers in Neuroscience 17 (July 10, 2023). http://dx.doi.org/10.3389/fnins.2023.1219025.

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Thanks to a more widespread knowledge of the disease, and improved diagnostic techniques, the clinical spectrum of cerebral amyloid angiopathy (CAA) is now broad. Sporadic CAA, hereditary CAA, CAA-related inflammation (CAA-ri) and iatrogenic CAA (iCAA) create a clinical and radiological continuum which is intriguing and only partially discovered. Despite being relatively rare, CAA-ri, an aggressive subtype of CAA with vascular inflammation, has gained growing attention also because of the therapeutic efficacy of anti-inflammatory and immunomodulating drugs. More recently, diagnostic criteria h

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Durrani, Romella, Meng Wang, Emily Cox, et al. "Mediators of Cognitive Impairment in Cerebral Amyloid Angiopathy." International Journal of Stroke, April 26, 2022, 174749302210993. http://dx.doi.org/10.1177/17474930221099352.

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Background Cerebral amyloid angiopathy (CAA) is associated with cognitive decline. CAA has diverse impacts on brain structure and function; however, the brain lesions that mediate the association of CAA with cognition are not understood well. Aims To determine the degree to which CAA neuroimaging biomarkers mediate the association of CAA with cognitive dysfunction. Methods We analyzed cross-sectional data of patients with probable CAA and controls without cognitive impairment from the Functional Assessment of Vascular Reactivity study. Neuropsychological tests were grouped into domains of memo

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Auriel, Eitan, Mahmut Edip Gurol, Jun Ni, et al. "Abstract W MP89: Validation of Clinical-Radiological Criteria for the Diagnosis of Cerebral Amyloid Angiopathy-related Inflammation." Stroke 45, suppl_1 (2014). http://dx.doi.org/10.1161/str.45.suppl_1.wmp89.

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Introduction: Cerebral amyloid angiopathy-related inflammation (CAA-ri) is a disease subtype characterized by rapidly progressive cognitive decline, seizures, headaches, T2-hyperintense MRI lesions, and neuropathologic evidence of CAA-associated vascular inflammation. CAA-ri is an important diagnosis to reach in clinical practice, as many patients respond to immunosuppressive therapy. Definitive diagnosis of CAA-ri generally requires brain biopsy, however, highlighting the importance of developing noninvasive diagnostic criteria. Objectives: To test the sensitivity and specificity of modified

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Gong, Xue, Liting Tang, Mei Wu, et al. "Development of a nomogram prediction model for early identification of persistent coronary artery aneurysms in kawasaki disease." BMC Pediatrics 23, no. 1 (2023). http://dx.doi.org/10.1186/s12887-023-03876-8.

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Abstract Background Coronary artery aneurysms (CAA) persistence prediction is critical in evaluating Kawasaki disease (KD). This study established a nomogram prediction system based on potential risk factors for assessing the risk of CAA persistence in a contemporary cohort of patients with KD. Methods This cohort comprised 105 patients with KD who had been diagnosed with CAA during the acute or subacute phase by echocardiography. The follow-up duration was at least 1 year. The clinical and laboratory parameters were compared between the CAA regression and persistence groups. Multivariable log

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Banerjee, Anik, Parisa Honarpisheh, Damian Gorski, Pedram Honarpisheh, Louise D. McCullough, and Juneyoung Lee. "Abstract 40: Gut Dysbiosis Exacerbates Neuroinflammation By Activation Of B Cells In A Mouse Model Of Cerebral Amyloid Angiopathy." Stroke 54, Suppl_1 (2023). http://dx.doi.org/10.1161/str.54.suppl_1.40.

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Introduction: Cerebral amyloid angiopathy (CAA) is a debilitating disease that leads to intracerebral hemorrhage, white matter disease, and progressive cognitive decline in patients >50 years of age. Studies investigating the neuroimmune landscape in CAA are sparse. Here, we investigate the role of B cells in CAA. Methods: Pre-symptomatic (2 months) and symptomatic (10-13 months) male Tg-SwDI mice (CAA mice) harboring Swedish, Dutch, and Iowa mutations of human amyloid precursor protein (APP) were used as a mouse model of CAA. Single cells isolated from the brain were analyzed using flow cy

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van Harten, Thijs, Anne Heijmans, Sanneke van Rooden, et al. "Brain Deep Medullary Veins on 7T MRI in Dutch-Type Hereditary Cerebral Amyloid Angiopathy." Journal of Alzheimer's Disease, September 16, 2022, 1–8. http://dx.doi.org/10.3233/jad-220354.

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Background: Deep medullary vein (DMV) changes occur in cerebral small vessel diseases (SVD) and in Alzheimer’s disease. Cerebral amyloid angiopathy (CAA) is a common SVD that has a high co-morbidity with Alzheimer’s disease. So far, DMVs have not been evaluated in CAA. Objective: To evaluate DMVs in Dutch-type hereditary CAA (D-CAA) mutation carriers and controls, in relation to MRI markers associated with D-CAA. Methods: Quantitative DMV parameters length, tortuosity, inhomogeneity, and density were quantified on 7 Tesla 3D susceptibility weighted MRI in pre-symptomatic D-CAA mutation carrier

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van Dort, Rosemarie, Kanishk Kaushik, Ingeborg Rasing, et al. "Cognition in (pre)symptomatic Dutch‐type hereditary and sporadic cerebral amyloid angiopathy." Alzheimer's & Dementia, October 10, 2024. http://dx.doi.org/10.1002/alz.14171.

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AbstractINTRODUCTIONCerebral amyloid angiopathy (CAA) is a main cause of cognitive dysfunction in the elderly. We investigated specific cognitive profiles, cognitive function in the stage before intracerebral hemorrhage (ICH), and the association between magnetic resonance imaging (MRI) based cerebral small vessel disease (cSVD) burden in CAA because data on these topics are limited.METHODSWe included Dutch‐type hereditary CAA (D‐CAA) mutation carriers with and without ICH, patients with sporadic CAA (sCAA), and age‐matched controls. Cognition was measured with a standardized test battery. Lin

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Muir, Ryan T., Sophie Stukas, Jennifer G. Cooper, et al. "Plasma biomarkers distinguish Boston Criteria 2.0 cerebral amyloid angiopathy from healthy controls." Alzheimer's & Dementia 21, no. 3 (2025). https://doi.org/10.1002/alz.70010.

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AbstractINTRODUCTIONCerebral amyloid angiopathy (CAA) is characterized by the deposition of beta‐amyloid (Aβ) in small vessels leading to hemorrhagic stroke and dementia. This study examined whether plasma Aβ42/40, phosphorylated‐tau (p‐tau), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) differ in CAA and their potential to discriminate Boston Criteria 2.0 probable CAA from healthy controls.METHODSPlasma Aβ42/40, p‐tau‐181, NfL, and GFAP were quantified using single molecule array (Simoa) and Aβ42/40 was also independently quantified using immunoprecipitation liqu

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