Journal articles: 'CAA'

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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 (January 22, 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 > CA3> CA11> CA2> CA6> CA10> CA7> CA4> CA5> CA9>CA8. Having the largest dipole moment the CA8 tautomer is expected to have the strongest interaction with polar solvents. The HF method calculated tautomeric equilibrium constants with respect to the most stable tautomer CA1 of Cyanuric acid both in the gas and in different solvents. The of the equilibrium constants calculated starting from the general outline of interconversion.

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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 (September 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 (Ca3, Ca4, and Ca5) were bound to the RTX parallel β-roll motif repeat structure (RTX domain). The metal ion (Ca2+) docking analysis gives a high binding energy, especially for Ca4 and Ca5 which are tightly bound to the RTX domain. The function of each Ca2+ ion is further analyzed using the MD simulation. The removal of Ca3, Ca4, and Ca5 caused the AMS8 lipase structure to become unstable and unfolded. The results suggested that Ca3, Ca4, and Ca5 stabilized the RTX domain. In conclusion, Ca3, Ca4, and Ca5 play a crucial role in the folding and stabilization of the RTX domain, which sustain the integrity of the overall AMS8 lipase structure.

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Mayo, Sherry. "CAA 2011." Visual Inquiry 1, no. 1 (August 24, 2011): 89–92. http://dx.doi.org/10.1386/vi.1.1.89_4.

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

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Cai, Shixuan, Hongyan Shi, Guoqian Li, Qilu Xue, Lei Zhao, Fu Wang, and Bo Hu. "3D-Printed Concentration-Controlled Microfluidic Chip with Diffusion Mixing Pattern for the Synthesis of Alginate Drug Delivery Microgels." Nanomaterials 9, no. 10 (October 12, 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 particle size can be influenced by channel length and flow rate ratio, which can be regulated to 448 nm in length and 235 nm in diameter. The delivery ratio of Doxorubicin (Dox) in CaA microgels are up to 90% based on the central stream strategy. CaA@Dox microgels with pH-dependent release property significantly enhances the cell killing rate against human breast cancer cells (MCF-7). The diffusion mixing pattern gives rise to well-controlled synthesis of CaA microgels, serving as a continuous and controllable production process for advanced drug delivery systems.

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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 (August 30, 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 months of the rearing period, the average body weight, shell height, and shell width of the snails reached the highest values in the Ca5 treatment (28.43 g, 54.97 mm, and 40.09mm, respectively) and these values were significantly different compared to the remaining calcium contents (Ca1, Ca3, Ca7, and Ca9). The survival rate of the snails in Ca3 (75.7%) was higher than in Ca1 and Ca7 (74.7%), Ca5 (73.7%), and Ca9 (71.7%). However, the survival rate was not significantly different among the treatments. Snails in Ca5 obtained the highest productivity (2.88 kg m-2) and this value was significantly different from Ca1 (2.55 kg m-2) and Ca9 (2.35 kg m-2). The results of this study showed that the growth rate and productivity of black apple snails were highest when they consumed a diet containing 5% calcium. The optimum requirement of calcium for the black apple snails in the grow-out period was 4.51%.

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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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Czach, Marie. "CAA in L.A." Afterimage 25, no. 6 (May 1998): 4–5. http://dx.doi.org/10.1525/aft.1998.25.6.4.

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Young, Cynthia. "Photography at CAA." Afterimage 27, no. 6 (May 2000): 7. http://dx.doi.org/10.1525/aft.2000.27.6.7.

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Han, Byung Hee, Meng-liang Zhou, Andrew W. Johnson, Itender Singh, Fan Liao, Ananth K. Vellimana, James W. Nelson, 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 (February 9, 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-derived ROS are a key mediator of CAA-induced CV deficits. First, the NADPH oxidase inhibitor, apocynin, and the nonspecific ROS scavenger, tempol, are shown to reduce oxidative stress and improve CV reactivity in aged Tg2576 mice. Second, the observed improvement in CV function is attributed both to a reduction in CAA formation and a decrease in CAA-induced vasomotor impairment. Third, anti-ROS therapy attenuates CAA-related microhemorrhage. A potential mechanism by which ROS contribute to CAA pathogenesis is also identified because apocynin substantially reduces expression levels of ApoE—a factor known to promote CAA formation. In total, these data indicate that ROS are a key contributor to CAA formation, CAA-induced vessel dysfunction, and CAA-related microhemorrhage. Thus, ROS and, in particular, NADPH oxidase-derived ROS are a promising therapeutic target for patients with CAA and AD.

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Rasing, Ingeborg, Sabine Voigt, Emma A. Koemans, Erik van Zwet, Paul C. de Kruijff, Thijs W. van Harten, Ellis S. van Etten, et al. "Occipital Cortical Calcifications in Cerebral Amyloid Angiopathy." Stroke 52, no. 5 (May 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) mutation or ≥1 lobar ICH and ≥1 first-degree relative with D-CAA and sporadic CAA patients with probable CAA according to the modified Boston criteria. D-CAA carriers were regarded symptomatic when they had a history of symptomatic ICH. We assessed the presence, location, and progression of calcifications and their association with ICH and the striped occipital cortex. Results: We found cortical calcifications in 15/81 (19% [95% CI, 11–29]) D-CAA mutation carriers (15/69 symptomatic and 0/12 presymptomatic) and in 1/59 (2% [95% CI, 0–9]) sporadic CAA patients. Calcifications were all bilateral located in the occipital lobes. In 3/15 (20%) of the symptomatic D-CAA patients the calcifications progressed over a period up to 10 years. There was evidence of an association between cortical calcifications and new ICH development (hazard ratio, 7.1 [95% CI, 0.9–54.9], log-rank P =0.03). In 7/25 D-CAA symptomatic carriers in whom a 7T-magnetic resonance imaging was performed, a striped pattern of the occipital cortex was present; in 3/3 (100%) of those with calcifications on computed tomography and 4/22 (18%) of those without calcifications. Conclusions: Occipital cortical calcifications are frequent in D-CAA but seem to be rare in sporadic CAA. Their absence in presymptomatic carriers and their association with ICH might suggest that they are a marker for advanced CAA. Cortical calcifications on computed tomography seem to be associated with the striped occipital cortex on 7T-magnetic resonance imaging which may possibly represent an early stage of calcification.

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Guidoux, Celine, Jean-Jacques Hauw, Isabelle F. Klein, Julien Labreuche, Claudine Berr, Charles Duyckaerts, and Pierre Amarenco. "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 hypertension. Postmortem 3D T2-weighted gradient-echo magnetic resonance imaging (MRI) with a 1.5-T magnet was performed in 11 brains with ICH (5 with CAA and 6 without) and histological correlation was performed when microbleeds were detected. Results: Hypertension and CAA were found in 69.1 and 24.7% of cases respectively. Among patients with CAA, 65.0% also had hypertension. The prevalence of CAA was similar among non-hypertensive cases and controls (33.3 and 23.1%; p = 0.54), whereas a significant difference was found between hypertensive cases vs. controls (28.9% vs. 0; p = 0.01). MRI documented 48 microbleeds and all 5 brains with CAA had ≥1 microbleed, compared to 3/6 brains without CAA. Among 48 microbleeds on MRI, 45 corresponded histologically to microbleeds surrounding microvessels (23 <200 µm in diameter, 19 between 200 µm and 2 mm, 3 were hemosiderin granules). Conclusions: Both hypertension and CAA frequently coexist in patients with ICH. MRI-detected microbleeds, proven by histological analysis, were twice as common in patients with CAA as in those with hypertensive ICH.

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Agnew, A., A. J. C. Fulford, N. De Jonge, F. W. Krijger, M. Rodriguez-Chacon, V. Gutsmann, and A. M. Deelder. "The relationship between worm burden and levels of a circulating antigen (CAA) of five species of Schistosoma in mice." Parasitology 111, no. 1 (July 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 levels were proportional to worm numbers: no density-dependent effects on CAA levels were observed even when mice carried worm burdens that were very large relative to host size. T-cell deprivation of the host had no effect on the CAA/worm burden relationship in either Schistosoma mansoni or S. haematobium infections and the CAA equilibrium was unaltered in intact mice when reduction of worm fecundity occurred. These data support the use of the CAA as an accurate and robust estimate of relative schistosome burden in man.

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Graff-Radford, Jonathan, Timothy G. Lesnick, Michelle M. Mielke, Eleni Constantopoulos, Alejandro A. Rabinstein, Scott A. Przybelski, Prashanthi Vemuri, et al. "Cerebral Amyloid Angiopathy Burden and Cerebral Microbleeds: Pathological Evidence for Distinct Phenotypes." Journal of Alzheimer's Disease 81, no. 1 (May 4, 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 relationship among CAA variables and performed principal component analysis (PCA) for dimension reduction to produce two scores from these 15 interrelated predictors. Hurdle models assessed relationships between principal components and lobar CMBs. Results: MRI-based CMBs appeared in 20/54 (37%). 10 participants had ≥2 lobar-only CMBs. The first two components of the PCA analysis of the CAA variables explained 74% variability. The first rotated component (RPC1) consisted of leptomeningeal and cortical CAA and the second rotated component of capillary CAA (RPC2). Both the leptomeningeal and cortical component and the capillary component correlated with lobar-only CMBs. The capillary CAA component outperformed the leptomeningeal and cortical CAA component in predicting lobar CMBs. Both capillary and the leptomeningeal/cortical components correlated with number of lobar CMBs. Conclusion: Capillary and leptomeningeal/cortical scores correlated with lobar CMBs on MRI but lobar CMBs were more closely associated with the capillary component. The capillary component correlated with APOE ɛ4, highlighting lobar CMBs as one aspect of CAA phenotypic diversity. More CMBs also increase the probability of underlying CAA.

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JIN, CHUNBO, BOYAN MAO, BAO LI, YUE FENG, DANDAN WU, JINSHENG XIE, and YOUJUN LIU. "HEMODYNAMIC STUDY OF CORONARY ARTERY ANEURYSMS." Journal of Mechanics in Medicine and Biology 20, no. 03 (April 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 exist in CAA. 2–7 times model: 1.1–14.4% reduction of blood flow downstream of CAA and 5, 7 times model showed upstream diastolic backward flow, the backward flow rate was 1.1% and 5.6%, respectively. The aveWSS at the CAA was 1.76–0.35[Formula: see text]Pa; the relative retention time was 1.1–14.6[Formula: see text]Pa[Formula: see text]; the average vorticity was 0.0085–231.7[Formula: see text]s[Formula: see text]. Conclusion:CAA can store blood, and the elasticity of the wall of CAA results in the flow of blood upstream. These two reasons make the downstream flow of CAA decrease and easily form intratumoral thrombosis, which may lead to myocardial ischemia.

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Tsai, Hsin-Hsi, Marco Pasi, Li-Kai Tsai, Chi-Ching Huang, Ya-Fang Chen, Bo-Ching Lee, Ruoh-Fang Yen, M. Edip Gurol, and Jiann-Shing Jeng. "Centrum Semiovale Perivascular Space and Amyloid Deposition in Spontaneous Intracerebral Hemorrhage." Stroke 52, no. 7 (July 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 small vessel disease–related ICH (non-CAA ICH). Clinical and image characteristics associated with high-degree perivascular spaces were evaluated in univariate and multivariable analyses. Univariate and multivariable models were performed to evaluate associations between the severity of perivascular spaces in CSO and amyloid retention in CAA-ICH and non–CAA-ICH cases. Results: Patients with CAA-ICH (n=29) and non–CAA-ICH (n=79) had similar prevalence of high-degree perivascular spaces in CSO (44.8% versus 36.7%; P =0.507) and in basal ganglia (34.5% versus 51.9%; P =0.131). High-degree perivascular spaces in CSO were independently associated with the presence of lobar microbleed (odds ratio, 3.0 [95% CI, 1.1–8.0]; P =0.032). The amyloid retention was higher in those with high-degree than those with low-degree CSO-perivascular spaces in CAA-ICH (global Pittsburgh compound B standardized uptake value ratio, 1.55 [1.33–1.61] versus 1.13 [1.01–1.48]; P =0.003) but not in non–CAA-ICH. In CAA-ICH, the association between cerebral amyloid retention and the degree of perivascular spaces in CSO remained significant after adjustment for age and lobar microbleed number ( P =0.004). Conclusions: Although high-degree magnetic resonance imaging–visible perivascular spaces are equally prevalent between CAA-ICH and non–CAA-ICH in the Asian cohort, the severity of magnetic resonance imaging–visible CSO-perivascular spaces may be an indicator of higher brain amyloid deposition in patients with CAA-ICH.

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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 (September 28, 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 are more favourable for research. In the past two decades, a variety of transgenic mouse models expressing the human Aβ 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.

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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 (December 15, 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 cases and literature data shows phenotypic heterogeneity of CAA and confirms advisability of routine use of paramagnetic conditions of MRT to examine patients with cerebrovascular disease.

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Barbato, Carmen, Piergiuseppe Liuzzi, Anna Maria Romoli, Francesca Draghi, Daniela Maccanti, Andrea Mannini, Claudio Macchi, Francesca Cecchi, and Bahia Hakiki. "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 (October 11, 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 enrolled for 12 months. Demographic and clinical data were recorded upon admission and discharge. Results: Among 102 sICH patients (age: 66 (IQR = 16), 53% female), 13% were diagnosed as probable/possible-CAA. TPO and functional assessment were comparable upon admission, but CAA patients were significantly older (p = 0.001). After a comparable LOS, CAA patients presented higher care burden (ERBI: p = 0.025), poorer functional recovery (FIM: p = 0.02) and lower levels of global independence (GOSE > 4: p = 0.03). In multivariate analysis, CAA was significantly correlated with a lower FIM (p = 0.019) and a lower likelihood of reaching GOS-E > 4, (p = 0.041) at discharge, independently from age. Conclusions: CAA seems to be independently associated with poorer rehabilitation outcomes, suggesting the importance of improving knowledge about CAA to better predict rehabilitation outcomes.

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Matsuda, Kana, Akihiro Shindo, Yuichiro Ii, Ken-ichi Tabei, Yukito Ueda, Hidehiro Ishikawa, Keita Matsuura, 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 (April 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 modified CAA-SVD score considering cortical microinfarcts and posterior dominant white matter hyperintensities, which are imaging findings of CAA, and examined the association between these scores and cognitive function in the same patient group.DesignProspective study.SettingSingle centre study from a memory clinic.ParticipantsSubjects were diagnosed with mild cognitive impairment (MCI) or mild dementia in our memory clinic between February 2017 and July 2019 and underwent clinical dementia rating scale and brain MRI assessment. A total of 42 patients (aged 75.3±9.12 years) were registered prospectively.Primary and secondary outcome measuresWe evaluated intellectual function, memory, frontal lobe function and constructional ability. Furthermore, the relationship between each score and cognitive function was examined.ResultsThe CAA-SVD score showed significant associations with cognitive function (R2=0.63, p=0.016), but the HA-SVD score did not (R2=0.41, p=0.35). The modified CAA-SVD score was also significantly associated with cognitive function (R2=0.65, p=0.008).ConclusionCognitive function is associated with the CAA-SVD score, and more efficiently with the modified CAA-SVD score, in memory clinic patients. Although we have not validated the weighting of the modified CAA-SVD score, these scores can be a predictor of cognitive deterioration in patients with MCI and mild dementia.

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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 examination, a whole coronal section of a cerebral hemisphere, at the level of the mamillary body, was taken for semiquantitative microscopic evaluation of the small cerebrovascular lesions.Results. CAA is present in 2/3% of the AD brains of which half of them have a severe form, grade 3. Only the latter displays more cerebrovascular lesions. CAA is present in 45% of the LBD brains. Cortical microinfarcts are only more frequent in the CAA grade 3 group. In LBD additional AD pathology is present in 41% of the CAA grade 0, 83% in grade 1-2, and 100% in grade 3. In PSP only 21% had CAA grade 1-2. In FTLD, CBD, and normal controls no CAA pathology is observed.Conclusions. The present study shows that CAA is most frequently associated to AD but that only the severe form displays more cerebrovascular lesions. LBD is the second most frequent disease associated to CAA with a clear correlation between the incidence of the associated AD features and the increasing severity of the CAA. In PSP only 21% display mild CAA features. PSP, tau-FTLD, and CBD are part of the Pick complex diseases, who are known to have a favourable vascular profile which can explain their low incidence of cerebrovascular lesions, in contrast to AD and LBD brains.

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Figura, Grzegorz, Edyta Koscianska, and Wlodzimierz Krzyzosiak. "In Vitro Expansion of CAG, CAA, and Mixed CAG/CAA Repeats." International Journal of Molecular Sciences 16, no. 8 (August 11, 2015): 18741–51. http://dx.doi.org/10.3390/ijms160818741.

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Li, Huadong, Hong Yu, Yu Song, Lu Tong, Meng Zhao, Anton V. Borovjagin, Nianguo Dong, and Long Wu. "Successful Surgical Treatment of a Giant Left Coronary Artery Aneurysm with Fistula." Heart Surgery Forum 24, no. 5 (October 7, 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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Wu, Zhiming, Chen Xu, Wei You, Fei Ye, and Xiangqi Wu. "Outcomes in Patients Fully Covered With Coronary Artery Aneurysm and Stenosis Lesion by Second Generation Drug-Eluting Stents After 1 Year." Angiology 71, no. 10 (July 28, 2020): 942–47. http://dx.doi.org/10.1177/0003319720944346.

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We evaluated the safety and efficacy of second-generation drug-eluting stents (DES) fully covering a coronary artery aneurysm (CAA) and stenosis lesion. Patients (n = 33) with CAA and stenosis lesion (>60%) were enrolled between January 2014 and December 2017. Baseline characteristics and biochemical variables were recorded during hospital admission. Changes in CAA resolution (the reduction on CAA size), minimal lumen diameter (MLD), and diameter stenosis (DS) were determined before, just after, and 1 year after percutaneous coronary intervention (PCI). After DES implantation, MLD and DS after PCI were improved compared with those before PCI ( P < .01). Also, thrombolysis in myocardial infarction blood flow was significantly enhanced after PCI ( P < .01). One year after PCI, maximal CAA diameter in patients with CAA and stenosis lesion was significantly reduced compared with those just after PCI ( P < .01). Meanwhile, CAA resolution ratio in these patients were more than those just after PCI ( P < .01). Furthermore, there was a significant reduction about CAA length in these patients ( P < .01). Last, there were no clinical events (including cardiac death, myocardial infarction, and revascularization) in the study. Second-generation DES implantation fully covering CAA and stenosis lesion was safe and effective.

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Nogueira, António, Francisco Peixoto, Maria Manuel Oliveira, Carlos André Pires, Bruno Colaço, Paula Alexandra Oliveira, and Maria João Pires. "The Effects of Long-Term Chaetomellic Acid A Administration on Renal Function and Oxidative Stress in a Rat Model of Renal Mass Reduction." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/5125980.

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Purpose.This study aimed to evaluate the effect of chronic treatment with chaetomellic acid A (CAA) on oxidative stress and renal function in a model of renal mass reduction.Methods. Male Wistar rats were subjected to 5/6 nephrectomy (RMR) or sham-operated (SO). One week after surgery, rats have been divided into four experimental groups: RMR: RMR rats without treatment(n=14); RMR + CAA: RMR rats treated with CAA(n=13); SO: SO rats without treatment(n=13); and SO + CAA: SO rats treated with CAA(n=13). CAA was intraperitoneally administered in a dose of 0.23 µg/Kg three times a week for six months.Results.RMR was accompanied by a significant reduction in catalase and glutathione reductase (GR) activity(p<0.05)and a decrease in reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio. CAA administration significantly increased catalase and GR activity(p<0.05)and increased GSH/GSSG ratio, but no significant difference between the treated and nontreated groups was found in this ratio. No significant differences were found between the RMR groups in any of the parameters of renal function. However, CAA administration slightly improves some parameters of renal function.Conclusions.These data suggest that CAA could attenuate 5/6 RMR-induced oxidative stress.

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Mehndiratta, Prachi, Sunil Manjila, Thomas Ostergard, Sylvia Eisele, Mark L. Cohen, Cathy Sila, and Warren R. Selman. "Cerebral amyloid angiopathy–associated intracerebral hemorrhage: pathology and management." Neurosurgical Focus 32, no. 4 (April 2012): E7. http://dx.doi.org/10.3171/2012.1.focus11370.

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Amyloid angiopathy–associated intracerebral hemorrhage (ICH) comprises 12%–15% of lobar ICH in the elderly. This growing population has an increasing incidence of thrombolysis-related hemorrhages, causing the management of hemorrhages associated with cerebral amyloid angiopathy (CAA) to take center stage. A concise reference assimilating the pathology and management of this clinical entity does not exist. Amyloid angiopathy–associated hemorrhages are most often solitary, but the natural history often progresses to include multifocal and recurrent hemorrhages. Compared with other causes of ICH, patients with CAA-associated hemorrhages have a lower mortality rate but an increased risk of recurrence. Unlike hypertensive arteriolar hemorrhages that occur in penetrating subcortical vessels, CAA-associated hemorrhages are superficial in location due to preferential involvement of vessels in the cerebral cortex and meninges. This feature makes CAA-associated hemorrhages easier to access surgically. In this paper, the authors discuss 3 postulates regarding the pathogenesis of amyloid hemorrhages, as well as the established clinicopathological classification of amyloid angiopathy and CAA-associated ICH. Common inheritance patterns of familial CAA with hemorrhagic strokes are discussed along with the role of genetic screening in relatives of patients with CAA. The radiological characteristics of CAA are described with specific attention to CAA-associated microhemorrhages. The detection of these microhemorrhages may have important clinical implications on the administration of anticoagulation and antiplatelet therapy in patients with probable CAA. Poor patient outcome in CAA-associated ICH is associated with dementia, increasing age, hematoma volume and location, initial Glasgow Coma Scale score, and intraventricular extension. The surgical management strategies for amyloid hemorrhages are discussed with a review of published surgical case series and their outcomes with a special attention to postoperative hemorrhage.

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Ii, Yuichiro, Hidehiro Ishikawa, Hirofumi Matsuyama, Akihiro Shindo, Keita Matsuura, Kimiko Yoshimaru, Masayuki Satoh, et al. "Hypertensive Arteriopathy and Cerebral Amyloid Angiopathy in Patients with Cognitive Decline and Mixed Cerebral Microbleeds." Journal of Alzheimer's Disease 78, no. 4 (December 8, 2020): 1765–74. http://dx.doi.org/10.3233/jad-200992.

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Background: Hypertensive arteriopathy (HA) and cerebral amyloid angiopathy (CAA) may contribute to the development of mixed cerebral microbleeds (CMBs). Recently, the total small vessel disease (SVD) scores for HA and CAA were proposed, which are determined by a combination of MRI markers to reflect overall severity of these microangiopathies. Objective: We investigated whether or not total HA-SVD and CAA-SVD scores could be used to predict overlap of HA and CAA in patients with mixed CMBs. Methods: Fifty-three subjects with mixed CMBs were retrospectively analyzed. MRI markers (CMBs, lacunes, perivascular space, white matter hyperintensity [WMH] and cortical superficial siderosis [cSS]) were assessed. The HA-SVD score and CAA-SVD score were obtained for each subject. Anterior or posterior WMH was also assessed using the age-related white matter changes scale. Results: The two scores were positively correlated (ρ= 0.449, p < 0.001). The prevalence of lobar dominant CMB distribution (p < 0.001) and lacunes in the centrum semiovale (p < 0.001) and the severity of WMH in the parieto-occipital lobes (p = 0.004) were significantly higher in the high CAA-SVD score group. cSS was found in four patients with high CAA-SVD score who showed lobar-dominant CMB distribution and severe posterior WMH. Conclusion: Mixed CMBs are mainly due to HA. Assessing both two scores may predict the overlap of HA and CAA in individuals with mixed CMBs. Patients with a high CAA-SVD score may have some degree of advanced CAA, especially when lobar predominant CMBs, severe posterior WMH, lobar lacunes, or cSS are observed.

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Fotiadis, Panagiotis, Yael D. Reijmer, Susanne J. Van Veluw, Sergi Martinez-Ramirez, Fikret Isik Karahanoglu, Elif Gokcal, Kristin M. Schwab, et al. "White matter atrophy in cerebral amyloid angiopathy." Neurology 95, no. 5 (July 1, 2020): e554-e562. http://dx.doi.org/10.1212/wnl.0000000000010017.

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ObjectiveWe postulated that cerebral amyloid angiopathy (CAA) is associated with white matter atrophy (WMA) and that WMA can be related to cognitive changes in CAA.MethodsWhite matter volume expressed as percent of intracranial volume (pWMV) of prospectively enrolled patients without dementia diagnosed with probable CAA was compared to age-matched healthy controls (HC) and patients with Alzheimer disease (AD). Cognitive scores were also sought to understand the potential effects of WMA on cognitive function.ResultsPatients with CAA (n = 72) had significantly lower pWMV (27.97% ± 2.63) when compared to age-matched HC (n = 72; mean difference [MD], 2.38%; p < 0.0001) and patients with AD (n = 72; MD, 1.57%; p < 0.0001). Differences were most pronounced in the posterior occipital regions in both comparisons. When comparisons were restricted to groups of patients with CAA but no intracerebral hemorrhage (n = 32) or hypertension (n = 32), and age-matched HC and AD, the significant differences were unaltered. Within the CAA cohort, higher age, lobar microbleed counts, and presence of hypertension were associated with lower pWMV (p = 0.0007, p = 0.031, and p = 0.003, respectively). All associations remained independent in multivariable analyses. Within the CAA cohort, higher pWMV independently correlated with better scores of executive function.ConclusionsPatients with CAA show WMA when compared to age-matched HC and patients with AD. WMA independently correlates with the number of lobar microbleeds, a marker of CAA severity. Consistent spatial patterns of WMA especially in posterior regions might be related to CAA. The association between WMA and measures of executive function suggests that WMA might represent an important mediator of CAA-related neurologic dysfunction.

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Charidimou, Andreas, Jan O. Friedrich, Steven M. Greenberg, and Anand Viswanathan. "Core cerebrospinal fluid biomarker profile in cerebral amyloid angiopathy." Neurology 90, no. 9 (January 31, 2018): e754-e762. http://dx.doi.org/10.1212/wnl.0000000000005030.

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ObjectiveTo perform a meta-analysis of 4 core CSF biomarkers (β-amyloid [Aβ]42, Aβ40, total tau [t-tau], and phosphorylated tau [p-tau]) to assess which of these are most altered in sporadic cerebral amyloid angiopathy (CAA).MethodsWe systematically searched PubMed for eligible studies reporting data on CSF biomarkers reflecting amyloid precursor protein metabolism (Aβ42, Aβ40), neurodegeneration (t-tau), and tangle pathology (p-tau) in symptomatic sporadic CAA cohorts vs controls and patients with Alzheimer disease (AD). Biomarker performance was assessed in random-effects meta-analysis based on ratio of mean (RoM) biomarker concentrations: (1) in patients with CAA vs healthy controls and (2) in patients with CAA vs patients with AD. RoM >1 indicates higher biomarker concentration in patients with CAA vs comparison population and RoM <1 indicates higher concentration in comparison groups.ResultsThree studies met inclusion criteria. These comprised 5 CAA patient cohorts (n = 59 patients) vs healthy controls (n = 94 cases) and AD cohorts (n = 158). Three core biomarkers differentiated CAA from controls: CSF Aβ42 (RoM 0.49, 95% confidence interval [CI] 0.38–0.64, p < 0.003), Aβ40 (RoM 0.70, 95% CI 0.63–0.78, p < 0.0001), and t-tau (RoM 1.54, 95% CI 1.15–2.07, p = 0.004); p-tau was marginal (RoM 1.24, 95% CI 0.99–1.54, p = 0.062). Differentiation between CAA and AD was strong for CSF Aβ40 (RoM 0.76, 95% CI 0.69–0.83, p < 0.0001), but not Aβ42 (RoM 1.00; 95% CI 0.81–1.23, p = 0.970). For t-tau and p-tau, average CSF ratios in patients with CAA vs patients with AD were 0.63 (95% CI 0.54–0.74, p < 0.0001) and 0.60 (95% CI 0.50–0.71, p < 0.0001), respectively.ConclusionSpecific CSF patterns of Aβ42, Aβ40, t-tau, and p-tau might serve as molecular biomarkers of CAA, but analyses in larger CAA cohorts are needed.

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Charidimou, Andreas, Karim Farid, Hsin-Hsi Tsai, Li-Kai Tsai, Rouh-Fang Yen, and Jean-Claude Baron. "Amyloid-PET burden and regional distribution in cerebral amyloid angiopathy: a systematic review and meta-analysis of biomarker performance." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 4 (October 25, 2017): 410–17. http://dx.doi.org/10.1136/jnnp-2017-316851.

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IntroductionWe performed a meta-analysis to synthesise current evidence on amyloid-positron emission tomography (PET) burden and presumed preferential occipital distribution in sporadic cerebral amyloid angiopathy (CAA).MethodsIn a PubMed systematic search, we identified case–control studies with extractable data on global and occipital-to-global amyloid-PET uptake in symptomatic patients with CAA (per Boston criteria) versus control groups (healthy participants or patients with non-CAA deep intracerebral haemorrhage) and patients with Alzheimer’s disease. To circumvent PET studies’ methodological variation, we generated and used ‘fold change’, that is, ratio of mean amyloid uptake (global and occipital-to-global) of CAA relative to comparison groups. Amyloid-PET uptake biomarker performance was then quantified by random-effects meta-analysis on the ratios of the means. A ratio >1 indicates that amyloid-PET uptake (global or occipital/global) is higher in CAA than comparison groups, and a ratio <1 indicates the reverse.ResultsSeven studies, including 106 patients with CAA (>90% with probable CAA) and 138 controls (96 healthy elderly, 42 deep intracerebral haemorrhage controls) and 72 patients with Alzheimer’s disease, were included. Global amyloid-PET ratio between patients with CAA and controls was above 1, with an average effect size of 1.18 (95% CI 1.08 to 1.28; p<0.0001). Occipital-to-global amyloid-PET uptake ratio did not differ between patients with CAA versus patients with deep intracerebral haemorrhage or healthy controls. By contrast, occipital-to-global amyloid-PET uptake ratio was above 1 in patients with CAA versus those with Alzheimer’s disease, with an average ratio of 1.10 (95% CI 1.03 to 1.19; p=0.009) and high statistical heterogeneity.ConclusionsOur analysis provides exploratory actionable data on the overall effect sizes and strength of amyloid-PET burden and distribution in patients with CAA, useful for future larger studies.

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Hirofuji, Aina, Azusa Furugen, Takeshi Kamada, Kenji Yamazaki, Hiroyuki Kamiya, and Hirosato Doi. "Giant Coronary Aneurysm with Coronary-Pulmonary Artery Fistula in a Jehovah's Witness." Thoracic and Cardiovascular Surgeon Reports 12, no. 01 (January 2023): e1-e3. http://dx.doi.org/10.1055/s-0042-1757877.

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AbstractWith an incidence of 3 in 100 million, giant coronary artery aneurysm (CAA) with coronary artery fistula (CAF) is a very rare condition. To prevent rupture, giant CAA with CAF should be swiftly treated. We present a Jehovah's Witness patient with giant CAA and coronary-pulmonary artery fistula. We resected the giant CAA in one piece, while ligating the CAF, without allogeneic blood transfusion. Due to rarity of these conditions, many thoracic surgeons lack direct experience in its surgical procedures. Herein, we share footage of this surgery as an example of how to safely resect CAA with minimal bleeding.

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Grysiewicz, Rebbeca, and Philip B. Gorelick. "Update on Amyloid-associated Intracerebral Hemorrhage." US Neurology 08, no. 01 (2012): 20. http://dx.doi.org/10.17925/usn.2012.08.01.20.

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Cerebral congophilic or amyloid angiopathy (CAA) is a clinicopathological entity that is considered a common cause of primary non-traumatic brain hemorrhage in the elderly. CAA is frequently associated with Alzheimers disease (AD) and has become a primary focus of scientific inquiry. The spectrum of intracerebral hemorrhage (ICH) that may occur in CAA includes: cerebral lobar hemorrhages, deep hemorrhages, purely subarachnoid and subdural hemorrhages and cerebral microbleeds. CAA is also associated with microinfarcts, leukoencephalopathy and superficial siderosis. This brief article will provide an update on the advances in our understanding of CAA-associated ICH with a focus on the following topics: neuropathology and mechanism of CAA-related hemorrhage; epidemiology, including genetic and other possible risk factors; clinical presentation; diagnosis, including newer imaging modalities; and prospects for prevention and treatment.

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Kulesh, A. A., N. Kh Gorst, V. E. Drobakha, N. A. Kaileva, A. Yu Bykova, and V. V. Shestakov. "Cerebral amyloid angiopathy, associated with inflammation: clinical observation and literature review." Perm Medical Journal 35, no. 6 (December 30, 2018): 53–60. http://dx.doi.org/10.17816/pmj35653-60.

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Cerebral amyloid angiopathy, associated with inflammation (CAA-I) is a rare syndrome, described rather long ago. The course of disease varies from conditionally asymptomatic, very seldom diagnosed forms to severe lethal cases with intracerebral bleedings and brain edema. The basic clinical symptoms of CAA-I are cognitive disorders, convulsions, headache, consciousness impairment, often ignored or wrong interpreted. Manifestations of CAA-I are a part of clinicoradiological continuum, significantly influencing the course of other cerebrovascular diseases. The paper presents description of a clinical case of symptom-free or preclinical form of CAA-I, incidentally detected while realizing magnetic resonance tomography. Analysis of this clinical case and literature data demonstrates difficulties of CAA-I differential diagnosis, value of neurovisualization in patients with cognitive disorders and accentuates the need of expanding the existing diagnostic criteria of CAA-I.

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Grysiewicz, Rebbeca, and Philip B. Gorelick. "Update on Amyloid-associated Intracerebral Haemorrhage." European Neurological Review 7, no. 1 (2012): 22. http://dx.doi.org/10.17925/enr.2012.07.01.22.

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Cerebral congophilic or amyloid angiopathy (CAA) is a clinicopathological entity that is considered a common cause of primary non-traumatic brain haemorrhage in the elderly. CAA is frequently associated with Alzheimer’s disease (AD) and has become a primary focus of scientific inquiry. The spectrum of intracerebral haemorrhage (ICH) that may occur in CAA includes: cerebral lobar haemorrhages, deep haemorrhages, purely subarachnoid and subdural haemorrhages and cerebral microbleeds. CAA is also associated with microinfarcts, leukoencephalopathy and superficial siderosis. This brief article will provide an update on the advances in our understanding of CAA-associated ICH with a focus on the following topics: neuropathology and mechanism of CAA-related haemorrhage; epidemiology, including genetic and other possible risk factors; clinical presentation; diagnosis, including newer imaging modalities; and prospects for prevention and treatment.

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Cisternas, Pablo, Xavier Taylor, and Cristian A. Lasagna-Reeves. "The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy." International Journal of Molecular Sciences 20, no. 24 (December 14, 2019): 6319. http://dx.doi.org/10.3390/ijms20246319.

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Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there is no clear understanding of the mechanisms underlying the contribution of CAA to neurodegeneration. Despite the fact that CAA is highly associated with the accumulation of Aβ, other types of amyloids have been shown to associate with the vasculature. Interestingly, in many cases, vascular amyloidosis has been associated with an active immune response and perivascular deposition of hyperphosphorylated tau. Despite the fact that in Alzheimer’s disease (AD) a major focus of research has been the understanding of the connection between parenchymal amyloid plaques, tau aggregates in the form of neurofibrillary tangles (NFTs), and immune activation, the contribution of tau and neuroinflammation to neurodegeneration associated with CAA remains understudied. In this review, we discussed the existing evidence regarding the amyloid diversity in CAA and its relation to tau pathology and immune response, as well as the possible contribution of molecular and cellular mechanisms, previously associated with parenchymal amyloid in AD and AD-related dementias, to the pathogenesis of CAA. The detailed understanding of the “amyloid-tau-neuroinflammation” axis in the context of CAA could open the opportunity to develop therapeutic interventions for dementias associated with CAA that are currently being proposed for AD and AD-related dementias.

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Matsuo, Ko, Akihiro Shindo, Atsushi Niwa, Ken-ichi Tabei, Hiroyasu Akatsu, Yoshio Hashizume, Haruhiko Akiyama, et al. "Complement Activation in Capillary Cerebral Amyloid Angiopathy." Dementia and Geriatric Cognitive Disorders 44, no. 5-6 (2017): 343–53. http://dx.doi.org/10.1159/000486091.

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Background: Cerebral amyloid angiopathy (CAA) is classified as type 1 with capillary amyloid β (Aβ) or type 2 without capillary Aβ. While it is known that CAA activates complement, an inflammatory mediator, there is no information on the relationship between capillary Aβ and complement activation. Methods: We evaluated 34 autopsy brains, including 22 with CAA and 12 with other neurodegenerative diseases. We assessed the vascular density of CAA by analyzing the expression of complement (C1q, C3d, C6, C5b-9), macrophage scavenger receptor (MSR), and apolipoprotein E (ApoE). Results: Capillary immunostaining for C1q, C3d, MSR, and ApoE was identified almost exclusively in CAA-type1 brains. There was intense expression of C1q, C3d, MSR, and ApoE, as well as weaker expression of C5b-9 and C6 in the arteries/ arterioles of both CAA subtypes, but not in control brains. C5b-9 and C6 were preferentially expressed in arteries/arterioles with subcortical hemorrhage or cortical superficial siderosis. Triple immunofluorescence revealed that C1q, C3d, and ApoE were colocalized with Aβ in CAA brain capillaries. Conclusion: Complement, MSR, and ApoE were only coexpressed in the presence of Aβ accumulation in capillaries, suggesting a role for complement activation in the propagation of Aβ. Additionally, C5b-9 expression may be associated with hemorrhagic brain injury in CAA.

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Ji, Jie, Peng Zhai, Wenhua Zheng, Zhi Suo, and Ying Xu. "A Laboratory Investigation into the Effects of Coarse Aggregate Angularity on Performance of WMA." Advances in Materials Science and Engineering 2018 (June 4, 2018): 1–11. http://dx.doi.org/10.1155/2018/1326945.

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This study evaluated the effects of coarse aggregate angularity (CAA) on the performances of warm mix asphalt (WMA) because previous studies have predominantly focused on the effects of CAA on the hot mix asphalt (HMA) performances. Five different CAAs were fabricated using Los Angeles abrasion test, and the digital image processing method was used to identify the CAA. Five mixes with different combinations of CAA and Sasobit-modified asphalt binder were prepared according to the Marshall mix design procedure. The performances such as the resistance to rutting and thermal cracking, moisture susceptibility, and volumetric characteristics of WMA were evaluated. The test results indicated that the CAA value was linearly declined with the abrasive wearing passes increased. Higher CAA value improved the potential to resistance to rutting of WMA but was not suitable to enhance the resistance to thermal cracking of WMA due to sharp corners that caused higher stress concentration. In addition, WMA was more prone to develop numerous macrocracking, which resulted in lower moisture susceptibility due to higher CAA value inducing higher air void, VMA, and VCA of WMA.

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Xiong, Yong, Ping Huang, and Qing-Gui Ren. "Transanal Pull-Through Procedure with Delayed versus Immediate Coloanal Anastomosis for Anus-Preserving Curative Resection of Lower Rectal Cancer: A Case-Control Study." American Surgeon 82, no. 6 (June 2016): 533–39. http://dx.doi.org/10.1177/000313481608200615.

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This case-control study compared the effectiveness and safety of transanal pull-through procedure (TPP) with delayed or immediate coloanal anastomosis (CAA) for anus-preserving curative resection of lower rectal cancer. Lower rectal cancer patients (n = 128) were hospitalized between January 2003 and December 2013 for elective anus-preserving curative resection through a TPP with delayed (n = 72) or immediate (n = 56) CAA. Main outcome measures including surgical safety, resection radicality, and defecation function were assessed. The two groups were comparable in age, sex, gross pathology, histology, and tumor-node-metastasis staging. Both the delayed and immediate CAA TPPs had similar resection radicality and safety profiles. The immediate CAA was associated with a significantly higher risk of anastomotic leakage and defecation impairment. None of patients in the delayed CAA group experienced anastomotic leakage. In conclusion, TPP with delayed CAA may be superior to immediate CAA in minimizing the risk of anastomotic leakage and relevant surgical morbidities, and does not require a temporary ileostomy and second-look restoration of ostomy.

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Hanner, Mary Anne. "CAA Update: 2008 Standards." Perspectives on Issues in Higher Education 10, no. 2 (October 2007): 10–11. http://dx.doi.org/10.1044/ihe10.2.10.

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Duman, I. E., V. A. Coenen, S. Doostkam, and H. Urbach. "Teaching Neuroimages: Inflammatory CAA." Clinical Neuroradiology 29, no. 2 (December 12, 2018): 379–82. http://dx.doi.org/10.1007/s00062-018-0750-9.

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Akkermans, R. A. D., P. Bernicke, R. Ewert, and J. Dierke. "From CAA to CFD." PAMM 16, no. 1 (October 2016): 617–18. http://dx.doi.org/10.1002/pamm.201610297.

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

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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 variants associated with h-CAA. Discussion; Although clinical exome testing was inconclusive, the presentation of CAA in two generations (mother and daughter) in their 8th and 7th decades respectively raises the possibility of a familial CAA rather than a sporadic CAA in this Indian family. Genome wide association studies are necessary to reveal if an Indian variant of familial CAA exists. We compare and contrast our familial CAA with the described h-CAA variants in the literature.

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Munsterman, Danielle, Sarina Falcione, Rebecca Long, Twinkle Joy, Mike Clarke, Andrew E. Beaudin, Richard Camicioli, Eric E. Smith, and Glen Jickling. "Abstract WP242: Transcriptomic Changes In Peripheral Blood Leukocytes Associated With The Cerebral Amyloid Angiopathy Small Vessel Disease Score." Stroke 54, Suppl_1 (February 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 evaluate changes in peripheral leukocyte gene expression associated with CAA severity. Methods: In 22 patients with CAA peripheral blood was collected into PAXgene tubes. RNA was isolated, and sequencing performed. Differentially expressed genes based on CAA small vessel disease (CAA-SVD) score as a marker of CAA severity were identified using ANOVA and functional pathway analysis. The relationship between leukocyte gene expression and CAA severity were assessed. Results: ANOVA was used to identify genes that were associated with CAA-SVD score (p≤0.05, partial correlation coefficient ≥;|0.5|). HDAC11, IL23A, TRAIL, TRAILR1 , TRAILR2 , and ICAM-1 were associated with CAA severity (CAA-SVD score). Canonical pathway analysis identified included induction of T lymphocytes, binding of antigen presentation cells, IL-12 signaling in macrophages/monocytes, activation of phagocytes, tight junction signaling, and activation of antigen presenting cells to be associated with CAA severity (p≤0.05). Conclusion: An association between the peripheral immune system and CAA severity was identified. Changes in neutrophil, monocyte, and Th17 cell gene expression in peripheral blood was associated with CAA severity. Further evaluation of immune system changes associated with CAA severity is needed to understand contribution to cerebral small vessel disease, cognitive decline, and potential roles as treatment targets or risk stratification markers in CAA.

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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 (April 28, 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 sections adjacent to the CAA for the segments with persistent CAA, at the former CAA and adjacent sections for those who regressed, and at various corresponding sections for segments with no history of CAA. Results: OCT was performed on 18 patients at 12.4 ± 5.5 years. Overall 14/18 (77.7%) had a history of CAA. Of those, 7/14 (50.0%) had regressed CAA at time of OCT. Data was analyzed according to echocardiographic and angiographic progress of CAA segments. Accordingly, all 18/18 persistent CAA segments and 11/11 regressed CAA segments had significant intimal hyperplasia, compared to 1/13 with no history of segmental CAA (P<0.001). The intensity of intimal hyperplasia is displayed in Table 1. Conclusion: Despite normal angiographic features, regressed CAA segments displayed significant intimal hyperplasia, similarly to those with persistent CAA. These features may present a risk of adverse coronary events.

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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 (July 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 without vascular deposition of Aβ (ADNC +/CAA −; so called, AD). Cerebral cortical vessels were isolated from FFPE sections using laser microdissection (LMD), processed by pressure cycling technology (PCT), and applied to SWATH (sequential window acquisition of all theoretical fragment ion spectra) proteomics. Results The protein expression levels of 17 proteins in ADNC +/CAA +/H donors (ADNC +/CAA + donors with highly abundant Aβ in capillaries) were significantly different from those in ADNC +/CAA − and ADNC −/CAA − donors. Furthermore, we identified 56 proteins showing more than a 1.5-fold difference in average expression levels between ADNC +/CAA + and ADNC −/CAA − donors, and were significantly correlated with the levels of Aβ or Collagen alpha-2(VI) chain (COL6A2) (CAA markers) in 11 donors (6 ADNC +/CAA + and 5 ADNC −/CAA −). Over 70% of the 56 proteins showed ADNC +/CAA + specific changes in protein expression. The comparative analysis with brain parenchyma showed that more than 90% of the 56 proteins were vascular-specific pathological changes. A literature-based pathway analysis showed that 42 proteins are associated with fibrosis, oxidative stress and apoptosis. This included the increased expression of Heat shock protein HSP 90-alpha, CD44 antigen and Carbonic anhydrase 1 which are inhibited by potential drugs against CAA. Conclusions The combination of LMD-based isolation of vessels from FFPE sections, PCT-assisted sample processing and SWATH analysis (FFPE-LMD-PCT-SWATH method) revealed for the first time the changes in the expression of many proteins that are involved in fibrosis, ROS production and cell death in ADNC +/CAA + (CAA patients) vessels. The findings reported herein would be useful for developing a better understanding of the pathology of CAA and for promoting the discovery and development of drugs and biomarkers for CAA.

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van den Berg, Emma, Johanna Nilsson, Iris Kersten, Gunnar Brinkmalm, Anna M. de Kort, Catharina J. M. Klijn, Floris H. B. M. Schreuder, 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 controls. Only neuronal pentraxin-2 levels were decreased in the CSF of CAA patients compared with controls (p = 0.04). CSF concentrations of 12 other synaptic proteins were all increased in AD compared with CAA or controls (all p≤0.01) and were unchanged between CAA and controls. Synaptic protein concentrations in the subgroup of CAA patients positive for AD biomarkers (CAA/ATN+; n = 6) were similar to AD patients, while levels in CAA/ATN- (n = 19) were comparable with those in controls. A regression model including all synaptic proteins differentiated CAA from AD at high accuracy levels (area under the curve 0.987). Conclusion: In contrast to AD, synaptic CSF biomarkers were found to be largely unchanged in CAA. Moreover, concomitant AD pathology in CAA is associated with abnormal synaptic protein levels. Impaired synaptic function in AD was confirmed in this independent cohort. Our findings support an apparent differential involvement of synaptic dysfunction in CAA and AD and may reflect distinct pathological mechanisms.

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Martinez-Ramirez, Sergi, Jose-Rafael Romero, M. Edip Gurol, Shoamanesh Ashkan, Ann C. McKee, Ellis van Etten, Octavio Pontes-Neto, 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 (February 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 was considered diagnostic of CAA. We excluded cases with: 1) non-lobar ICH; 2) alternative clinical diagnosis for the lobar hemorrhage/es; 3) CAA-negative studies based on small brain biopsy samples (greater diameter <1 cm) or clot evacuations with none or rare vessels identified; 4) autopsy studies not grading CAA. We determined sensitivity and specificity of “possible CAA” (1 lobar hemorrhage) and “probable CAA” (>1 strictly lobar hemorrhage) in both cohorts. Results: The study included 143 cases: 96 from the hospital cohort (mean age at time of MRI 74.1±8.2 years, 47.9% women, 47.9% autopsy studies, 54.2% cases with any lobar microbleed, 44.8% with any lobar ICH) and 47 from FHS (mean age at time of MRI 83.4±10.9 years, 48.9% women, 100% autopsy studies, 17% cases with any lobar microbleed, no lobar ICH cases). Hospital cohort: CAA prevalence was 72.6%. Specificity/sensitivity of “possible CAA” and “probable CAA” were 78.2%/33.3% and 92%/57.7%. Community cohort: CAA prevalence was 47%. Specificity/sensitivity of “probable CAA” were 88%/3%. Discussion: Specificity of detection of multiple lobar hemorrhages on MRI (“probable CAA”) for moderate-severe CAA is similarly high in both hospital and community cohorts. This increases the opportunity to identify individuals with CAA for observational studies and emerging anti-amyloid therapeutic trials. In view of its poor sensitivity, “probable CAA” diagnosis represents an inadequate screening tool for exclusion of CAA in both populations.

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Journal articles on the topic 'CAA'

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