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caa cerebral amyloid angiopathy young

Muhammad Taimur Malik, Corey Myers, Syed Jaffar Kazmi, Ramin Zand
Cerebral Amyloid Angiopathy (CAA) is one of the significant causes of lobar intracerebral hemorrhage (ICH) mainly among elderly people. Sporadic cases of CAA have been linked to genetic polymorphisms with an increased risk of disease, an earlier presentation, and an accelerated pathology [1]. Here, we present a patient with no significant risk factors who had a recurrent intracerebral hemorrhage secondary to CAA probably induced by exercise.
December 2017: Journal of Vascular and Interventional Neurology
André Caetano, Filipa Ladeira, Raquel Barbosa, Sofia Calado, Miguel Viana-Baptista
BACKGROUND: Early identification of patients with cerebral amyloid angiopathy (CAA) is relevant considering the increased risk for cerebral hemorrhage. A new set of diagnostic criteria for CAA was recently proposed, which include the presence of superficial siderosis. We aimed to assess the impact of applying these criteria regarding use of antithrombotic therapy. METHODS: Review of consecutive patients admitted to a Neurology Department from 2014 to 2016, with acute parenchymal or subarachnoid hemorrhage and/or atypical transient focal neurological episodes...
January 15, 2018: Journal of the Neurological Sciences
Young Kyoung Jang, Hee Jin Kim, Jin San Lee, Yeo Jin Kim, Ko Woon Kim, Yeshin Kim, Hyemin Jang, Juyoun Lee, Jong Min Lee, Seung-Joo Kim, Kyung-Ho Yu, Andreas Charidimou, David J Werring, Sung Tae Kim, Duk L Na, Sang Won Seo
Restricted lobar cerebral microbleeds (CMBs) and cortical superficial siderosis (CSS) are the characteristic markers of cerebral amyloid angiopathy (CAA). However, their effects on clinical features has not been evaluated well. The purpose of this study is to investigate the clinical implication of these markers in clinical-radiologically diagnosed CAA. A total of 372 patients with possible or probable CAA who met the modified Boston criteria were recruited in a memory clinic setting. Cortical thickness was measured using surface based methods...
November 22, 2017: Scientific Reports
Hee Jin Kim, Hanna Cho, David J Werring, Young Kyoung Jang, Yeo Jin Kim, Jin San Lee, Juyoun Lee, Soomin Jun, Seongbeom Park, Young Hoon Ryu, Jae Yong Choi, Young Seok Cho, Seung Hwan Moon, Duk L Na, Chul Hyoung Lyoo, Sang Won Seo
Cerebrovascular deposition of amyloid-β, known as cerebral amyloid angiopathy (CAA), is associated with MRI findings of lobar hemorrhage, cerebral microbleeds, and cortical superficial siderosis. Although pathological studies suggest that tau may co-localize with vascular amyloid, this has not yet been investigated in CAA in vivo. Three patients with probable CAA underwent 11C-Pittsburgh Compound B (PiB) PET or 18F-florbetaben PET to evaluate amyloid burden, and 18F-AV-1451 PET to evaluate paired helical filament tau burden...
2017: Journal of Alzheimer's Disease: JAD
Yoichi Nakayama, Yohei Mineharu, Yoshiki Arawaka, Sei Nishida, Hirofumi Tsuji, Hidehiko Miyake, Maki Yamaguchi, Sachiko Minamiguchi, Yasushi Takagi, Susumu Miyamoto
Cerebral amyloid angiopathy (CAA), a cause of recurrent and multiple lobar hemorrhages, characteristically occurs in persons aged ≥55 years. We report a case of a 32-year-old male who had recurrent hemorrhage in the left multiple lobes, with a history of traumatic brain injury and hematoma evacuation at the age of 1 year. He underwent surgical treatment and was histopathologically diagnosed as having CAA. The literature review yielded six CAA cases, including ours, aged less than 55 years. All were male and four had histories of severe TBI, suggesting that male sex and TBI may be associated with CAA in young persons...
January 2017: Acta Neurochirurgica
A Manousopoulou, M Gatherer, C Smith, J A R Nicoll, C H Woelk, M Johnson, R Kalaria, J Attems, S D Garbis, R O Carare
AIMS: Amyloid beta (Aβ) accumulation in the walls of leptomeningeal arteries as cerebral amyloid angiopathy (CAA) is a major feature of Alzheimer's disease. In this study, we used global quantitative proteomic analysis to examine the hypothesis that the leptomeningeal arteries derived from patients with CAA have a distinct endophenotypic profile compared to those from young and elderly controls. METHODS: Freshly dissected leptomeningeal arteries from the Newcastle Brain Tissue Resource and Edinburgh Sudden Death Brain Bank from seven elderly (82...
October 2017: Neuropathology and Applied Neurobiology
Hae-Won Koo, Kyung-Il Jo, Je-Young Yeon, Jong-Soo Kim, Seung-Chyul Hong
BACKGROUND: There is no doubt that cerebral amyloid angiopathy (CAA) is a key risk factor for recurrent lobar ICH, however, the exact mechanism and interaction with MRI markers of disease severity are less well known. Centrum semiovale-perivascular spaces (CSO-PVS) have been suggested as adjunctive diagnostic criteria in order to enhance diagnostic power. The purposes of this study were to investigate the prevalence of CSO-PVS and its association with other imaging signatures {lobar microbleeds (CMB), cortical superficial siderosis (CSS), white matter hyperintensity (WMH)} in lobar ICH patients as well as recurrent lobar ICH risk, especially in patients taking antithrombotic agents...
August 15, 2016: Journal of the Neurological Sciences
Y C Chung, A Kruyer, Y Yao, E Feierman, A Richards, S Strickland, E H Norris
UNLABELLED: Essentials Evidence suggests a comorbidity between hyperhomocysteinemia (HHC) and Alzheimer's disease (AD). Homocysteine (HC) could affect the β-amyloid (Aβ)-fibrinogen interaction in AD pathology. AD patients with concomitant HHC have increased fibrin and Aβ deposits in their brains. HC contributes to AD pathology via the Aβ-fibrinogen interaction. SUMMARY: Background Accumulating clinical evidence suggests that hyperhomocysteinemia (HHC) is correlated with Alzheimer's disease (AD) and vascular dementia...
July 2016: Journal of Thrombosis and Haemostasis: JTH
Xiaoying Chong, Xian Lu, Yu Wang, Alan K Chang, Linan Xu, Na Wang, Yonghui Sun, Gary W Jones, Youtao Song, Yong-Bo Song, Jianwei He
Human cystatin C (HCC) amyloid angiopathy (HCCAA) is characterized by tissue deposition of amyloid fibrils in blood vessels, which can lead to recurrent hemorrhagic stroke. Wild-type HCC forms part of the amyloid deposits in brain arteries of elderly people with amyloid angiopathy. A point mutation causing a glutamine to a leucine substitution at residue 68 in the HCC polypeptide chain greatly increases the amyloidogenic propensity of HCC and causes a more severe cerebral hemorrhage and premature death in young adults...
December 2016: Journal of Biomolecular Structure & Dynamics
Karim Farid, Young T Hong, Franklin I Aigbirhio, Tim D Fryer, David K Menon, Elizabeth A Warburton, Jean-Claude Baron
Although late-phase (>35min post-administration) 11C-PiB-PET has good sensitivity in cerebral amyloid angiopathy (CAA), its specificity is poor due to frequently high uptake in healthy aged subjects. By detecting perfusion-like abnormalities, early-phase 11C-PiB-PET might add diagnostic value. Early-frame (1-6min) 11C-PiB-PET was obtained in 11 non-demented patients with probable CAA-related symptomatic lobar intracerebral haemorrhage (70±7yrs), 9 age-matched healthy controls (HCs) and 10 HCs <55yrs...
2015: PloS One
Sherri A Braksick, James P Klaas, Robert D Brown, Alejandro A Rabinstein, Sara E Hocker, Jennifer E Fugate
BACKGROUND: To determine the influence of antithrombotic use on the etiology of primary intracerebral hemorrhage (ICH). METHODS: We conducted a retrospective review of consecutive patients admitted with primary ICH from 2009 to 2012. Data recorded included age, history of hypertension, and use of antithrombotic medications. Imaging was reviewed to determine hemorrhage location and the presence and the location of any microhemorrhages. Etiologies were classified using a predetermined algorithm, which was based on existing literature...
March 2015: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Roy O Weller, Cheryl A Hawkes, Raj N Kalaria, David J Werring, Roxana O Carare
White matter abnormalities on magnetic resonance imaging (MRI) are associated with dementia and include white matter hyperintensities (WMH; also termed leukoaraiosis) and visible perivascular spaces (PVS). We review the potential role of impaired drainage of interstitial fluid in the pathogenesis of WMH and PVS. Whereas the volume of extracellular space in the grey matter is tightly controlled, fluid accumulates and expands the extracellular spaces of the white matter in acute hydrocephalus, vasogenic edema and WMH...
January 2015: Brain Pathology
Eric Milner, Meng-Liang Zhou, Andrew W Johnson, Ananth K Vellimana, Jacob K Greenberg, David M Holtzman, Byung Hee Han, Gregory J Zipfel
BACKGROUND AND PURPOSE: We and others have shown that soluble amyloid β-peptide (Aβ) and cerebral amyloid angiopathy (CAA) cause significant cerebrovascular dysfunction in mutant amyloid precursor protein (APP) mice, and that these deficits are greater in aged APP mice having CAA compared with young APP mice lacking CAA. Amyloid β-peptide in young APP mice also increases infarction after focal cerebral ischemia, but the impact of CAA on ischemic brain injury is unknown. METHODS: To determine this, we assessed cerebrovascular reactivity, cerebral blood flow (CBF), and extent of infarction and neurological deficits after transient middle cerebral artery occlusion in aged APP mice having extensive CAA versus young APP mice lacking CAA (and aged-matched littermate controls)...
October 2014: Stroke; a Journal of Cerebral Circulation
Jean-Claude Baron, Karim Farid, Eamon Dolan, Guillaume Turc, Siva T Marrapu, Eoin O'Brien, Franklin I Aigbirhio, Tim D Fryer, David K Menon, Elizabeth A Warburton, Young T Hong
By detecting β-amyloid (Aβ) in the wall of cortical arterioles, amyloid positron emission tomography (PET) imaging might help diagnose cerebral amyloid angiopathy (CAA) in patients with lobar intracerebral hemorrhage (l-ICH). No previous study has directly assessed the diagnostic value of (11)C-Pittsburgh compound B (PiB) PET in probable CAA-related l-ICH against healthy controls (HCs). (11)C-PiB-PET and magnetic resonance imaging (MRI) including T2* were obtained in 11 nondemented patients fulfilling the Boston criteria for probable CAA-related symptomatic l-ICH (sl-ICH) and 20 HCs without cognitive complaints or impairment...
May 2014: Journal of Cerebral Blood Flow and Metabolism
Nina S Gowert, Lili Donner, Madhumita Chatterjee, Yvonne S Eisele, Seyda T Towhid, Patrick Münzer, Britta Walker, Isabella Ogorek, Oliver Borst, Maria Grandoch, Martin Schaller, Jens W Fischer, Meinrad Gawaz, Sascha Weggen, Florian Lang, Mathias Jucker, Margitta Elvers
Alzheimer's disease (AD) is characterized by neurotoxic amyloid-ß plaque formation in brain parenchyma and cerebral blood vessels known as cerebral amyloid angiopathy (CAA). Besides CAA, AD is strongly related to vascular diseases such as stroke and atherosclerosis. Cerebrovascular dysfunction occurs in AD patients leading to alterations in blood flow that might play an important role in AD pathology with neuronal loss and memory deficits. Platelets are the major players in hemostasis and thrombosis, but are also involved in neuroinflammatory diseases like AD...
2014: PloS One
Seiji Ohtani, Keiko Shimizu, Masaru Asari, Chikatoshi Maseda, Kumiko Oka, Hiromi Yamada, Chisato Hoshina, Hiroki Doi, Daisuke Yajima, Hiroshi Shiono, Katsuhiro Ogawa
We report findings from an autopsy of a male in his 40s who died of a brain stem hemorrhage associated with cerebral amyloid angiopathy (CAA), senile plaques (SPs) and neurofibrillary tangles (NFTs), which are histopathological changes associated with Alzheimer's disease (AD). Our immunohistochemical study demonstrated amyloid β (Aβ) deposition in the small cerebral arteries and SPs. Although hypertension (178/132 mmHg) was detected, the subject was not treated accordingly. CAA coupled with hypertension might have caused the intracerebral hemorrhage (ICH)...
March 2014: Legal Medicine
Carlo Salvarani, Gene G Hunder, Jonathan M Morris, Robert D Brown, Teresa Christianson, Caterina Giannini
OBJECTIVE: To analyze the clinical findings, response to therapy, and outcomes of patients with cerebral vascular amyloid-β (Aβ) deposition with and without inflammatory vascular infiltration. METHODS: We report 78 consecutive patients with cerebral vascular Aβ deposition examined at Mayo Clinic Rochester over 25 years (1987 through 2011). Specimens reviewed by a neuropathologist showed 40 with vascular Aβ peptide without inflammation (cerebral amyloid angiopathy [CAA]), 28 with granulomatous vasculitis (Aβ-related angiitis or ABRA), and 10 with perivascular CAA-related inflammation...
October 29, 2013: Neurology
Dietmar Rudolf Thal, Christine von Arnim, W Sue T Griffin, Haruyasu Yamaguchi, Robert E Mrak, Johannes Attems, Ajeet Rijal Upadhaya
Alzheimer's disease (AD) is characterized neuropathologically by the presence of amyloid plaques, neuritic plaques, and neurofibrillary tangles (NFTs). These lesions occur not only in demented individuals with AD but also in non-demented persons. In non-demented individuals, amyloid and neuritic plaques are usually accompanied with NFTs and are considered to represent asymptomatic or preclinical AD (pre-AD) pathology. Here, we defined and characterized neuropathological differences between clinical AD, non-demented pre-AD, and non-AD control cases...
November 2013: European Archives of Psychiatry and Clinical Neuroscience
Jae-Hyun Park, Sang Won Seo, Changsoo Kim, Geon Ha Kim, Hyun Jin Noh, Sung Tae Kim, Ki-Chang Kwak, Uicheul Yoon, Jong Min Lee, Jong Weon Lee, Ji Soo Shin, Chi Hun Kim, Young Noh, Hanna Cho, Hee Jin Kim, Cindy W Yoon, Seung Jun Oh, Jae Seung Kim, Yearn Seong Choe, Kyung-Han Lee, Jae-Hong Lee, Michael Ewers, Michael W Weiner, David J Werring, Duk L Na
OBJECTIVE: Cerebral microbleeds (CMBs) are a neuroimaging marker of small vessel disease (SVD) with relevance for understanding disease mechanisms in cerebrovascular disease, cognitive impairment, and normal aging. It is hypothesized that lobar CMBs are due to cerebral amyloid angiopathy (CAA) and deep CMBs are due to subcortical ischemic SVD. We tested this hypothesis using structural magnetic resonance imaging (MRI) markers of subcortical SVD and in vivo imaging of amyloid in patients with cognitive impairment...
May 2013: Annals of Neurology
Rob J A Nabuurs, Remco Natté, Fenna M de Ronde, Ingrid Hegeman-Kleinn, Jouke Dijkstra, Sjoerd G van Duinen, Andrew G Webb, Annemieke J Rozemuller, Mark A van Buchem, Louise van der Weerd
Cerebral deposits of amyloid-β peptides (Aβ) form the neuropathological hallmarks of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). In the brain, Aβ can aggregate as insoluble fibrils present in amyloid plaques and vascular amyloid, or as diffuse plaques consisting of mainly non-fibrillar Aβ. Previously, magnetic resonance imaging (MRI) has been shown to be capable of detecting individual amyloid plaques, not only via the associated iron, but also Aβ itself has been suggested to be responsible for a decrease in the image intensity...
2013: Journal of Alzheimer's Disease: JAD
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