標題: Titlebook: Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders; Marcel M. Verbeek,Robert M. W. Waal,Harry V. Vinte Book 2000 Spr [打印本頁] 作者: Aggrief 時間: 2025-3-21 17:11
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders影響因子(影響力)
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders影響因子(影響力)學(xué)科排名
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders網(wǎng)絡(luò)公開度
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders網(wǎng)絡(luò)公開度學(xué)科排名
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders被引頻次
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders被引頻次學(xué)科排名
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders年度引用
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders年度引用學(xué)科排名
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders讀者反饋
書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders讀者反饋學(xué)科排名
作者: 香料 時間: 2025-3-22 00:14 作者: 幼稚 時間: 2025-3-22 01:05 作者: Electrolysis 時間: 2025-3-22 07:51 作者: freight 時間: 2025-3-22 12:12
Einführung in Teil II: Forschungsergebnisseenhanced but plaque formation is not essentially associated with neurofibrillary degeneration. Evidence suggests similarities between early events in the development of cerebral amyloid angiopathy and senile plaques.作者: wreathe 時間: 2025-3-22 16:35
https://doi.org/10.1007/978-3-658-40652-3top codon normally occurring in the precursor molecule and a longer open-reading frame of 277 amino acids instead of 266. The two most characteristic microscopic lesions of PrP-CAA and FBD are amyloid deposits in parenchymal blood vessels and neurofibrillary lesions.作者: wreathe 時間: 2025-3-22 20:22 作者: Invigorate 時間: 2025-3-22 22:45
Chemical Analysis of Amyloid β Protein in CAAciation of vascular Aβ with other proteins, carbohydrates and lipids results in additional amyloid stability. There appears to be a strong positive correlation between the magnitude of Aβ. deposition and the dosage of apolipoprotein E4.作者: 陰險 時間: 2025-3-23 04:08 作者: VEST 時間: 2025-3-23 06:20 作者: Barrister 時間: 2025-3-23 11:04
Neuropathology and Genetics of Prion Protein and British Cerebral Amyloid Angiopathiestop codon normally occurring in the precursor molecule and a longer open-reading frame of 277 amino acids instead of 266. The two most characteristic microscopic lesions of PrP-CAA and FBD are amyloid deposits in parenchymal blood vessels and neurofibrillary lesions.作者: arthrodesis 時間: 2025-3-23 15:30
Amyloid β Protein Internalization and Production by Canine Smooth Muscle Cells underlying the development of cerebrovascular Aβ deposition. This review summarizes the results obtained with canine SMC cultures and discusses their potential implications for the pathogenesis of CAA.作者: bronchiole 時間: 2025-3-23 20:54 作者: Radiation 時間: 2025-3-23 22:16 作者: 埋伏 時間: 2025-3-24 05:51 作者: Harbor 時間: 2025-3-24 08:44 作者: glomeruli 時間: 2025-3-24 14:40
Cerebral Microvascular and Macrovascular Disease in the Aging Brain; Similarities and Differenceselium, pericytes and (less likely) macrophages may play a central role in causation of many forms of vasculopathy, including CAA. . and animal (including transgenic) models may have a part in elucidating their origins and eventual treatment.作者: 航海太平洋 時間: 2025-3-24 18:00
Book 2000time seems right for a book whichexamines the phenomenon of CAA using a multifaceted approach: Whatdoes it produce clinically? How might CAA be imaged? What are thecrucial biochemical/cellular events within cerebral vessel walls thatlead to CAA? How can .in vitro. or transgenic experimental systemsb作者: STALE 時間: 2025-3-24 19:32 作者: 無思維能力 時間: 2025-3-24 23:42
Analysis of In-Plane Loading - Case Studies,eased tendency to dimerize, aggregate and form amyloid depositions, primarily in the walls of small arteries and arterioles of the brain. In the following chapter the epidemiology, clinical aspects, pathology, molecular biology and pathophysiology of HCCAA are reviewed.作者: 頑固 時間: 2025-3-25 06:24 作者: Cuisine 時間: 2025-3-25 08:42
Vascular Risk Factors for Alzheimer’s Diseased Alzheimer’s disease, and that the presence of cerebrovascular disease intensifies the presence and severity of the clinical symptoms of Alzheimer’s disease. In this chapter, current knowledge on the relation between vascular risk factors and Alzheimer’s disease is reviewed.作者: 性冷淡 時間: 2025-3-25 11:58 作者: Flagging 時間: 2025-3-25 16:41
Diagnosis of CAA during Lifey strategy. In pursuit of this, animal studies have demonstrated the feasibility to deliver monoclonal antibodies and peptides to the brain. Physiological transport mechanisms for some peptides (transferrin, insulin and others) are present at the barrier and were utilized to transport radiolabeled a作者: 夸張 時間: 2025-3-25 22:52 作者: 割公牛膨脹 時間: 2025-3-26 00:22 作者: cacophony 時間: 2025-3-26 08:03 作者: intercede 時間: 2025-3-26 11:48
Blood Brain Barrier Dysfunction and Cerebrovascular Degeneration in Alzheimer’s Diseasel and morphological evidence in context with the variable but distinct cerebrovascular pathology described to be associated with AD. I also consider genetic influences such as apolipoprotein E in relation to cerebrovascular lesions that may shed light on the pathophysiology of the cerebral vasculatu作者: DECRY 時間: 2025-3-26 13:44 作者: 細絲 時間: 2025-3-26 20:09 作者: Aggressive 時間: 2025-3-27 00:50
https://doi.org/10.1007/978-3-658-40308-9ng a complex relationship between . ε4, . ε2 and hemorrhage associated with CAA. For example, pathological studies have demonstrated that the . ε2 allele, the least frequent of the . alleles, is over-represented in patients with CAA-related hemorrhage. This is also true for patients with co-existing作者: 規(guī)范就好 時間: 2025-3-27 01:26 作者: MAL 時間: 2025-3-27 05:22
André Kieserling,Martin Wei?mannyloid-associated proteins in the basement membrane precedes focal Aβ. deposition. Initial Aβ. deposits may be a seed for further massive deposition of Aβ. (leading to advanced CAA) in both meningeal and cortical vessels.作者: 搖擺 時間: 2025-3-27 12:25
Dennis Ahrholdt,Goetz Greve,Gregor Hopfl and morphological evidence in context with the variable but distinct cerebrovascular pathology described to be associated with AD. I also consider genetic influences such as apolipoprotein E in relation to cerebrovascular lesions that may shed light on the pathophysiology of the cerebral vasculatu作者: 寄生蟲 時間: 2025-3-27 16:51
Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders作者: progestogen 時間: 2025-3-27 21:15 作者: 頭盔 時間: 2025-3-27 22:54
Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders978-94-017-1007-7作者: 貞潔 時間: 2025-3-28 04:42
Kombinatorische Optimierungsprobleme. Though fundamentally a neuropathologic diagnosis, CAA can be identified with good reliability during life by the presence on gradient-echo MRI of multiple, strictly lobar hemorrhages without other definite cause. The relatively good recovery from a first CAA-related hemorrhage is counterbalanced b作者: 離開可分裂 時間: 2025-3-28 07:13 作者: CERE 時間: 2025-3-28 10:27
Kombinatorische Optimierungsproblement occurrence of these two disorders is not a rare phenomenon. In recent years, evidence is increasing that the two may be more closely linked than just by chance. Epidemiological studies have suggested that the risk factors for vascular disease and stroke are associated with cognitive impairment an作者: accomplishment 時間: 2025-3-28 15:48
https://doi.org/10.1007/978-3-658-40087-3sider non-CAA forms of vasculopathy. Specifically, similarities and differences between atherosclerosis and small artery lesions (arteriosclerosis/lipohyalinosis, CADASIL, Binswanger’s subcortical leukoencephalopathy, HERNS) will be discussed in terms of their clinicopathologic manifestations and pu作者: 加入 時間: 2025-3-28 22:11
https://doi.org/10.1007/978-3-658-40308-9 transport and metabolism. Following genetic linkage of late-onset familial Alzheimer’s disease to chromosome 19 and the identification of ApoE in senile plaques, neurofibrillary tangles and amyloid-laden blood vessels, over-representation of the . ε4 allele was recognized in both familial late-onse作者: 演繹 時間: 2025-3-29 00:56 作者: 爵士樂 時間: 2025-3-29 04:28
Analysis of In-Plane Loading - Case Studies,otide substitution in the gene encoding the cysteine proteinase inhibitor, cystatin C, gives rise to a structurally unstable variant protein with increased tendency to dimerize, aggregate and form amyloid depositions, primarily in the walls of small arteries and arterioles of the brain. In the follo作者: refine 時間: 2025-3-29 08:37
Organisationen nachhaltig bewegen consequences of CAA in the brain; especially cerebral hemorrhage. Specifically, we will evaluate the relationship between sporadic CAA and that related to Alzheimer disease, unique neuropathologie features of CAA-related brain hemorrhage, and introduce the concept of CAA-associated microangiopathie作者: 代替 時間: 2025-3-29 14:07
Organisationen nachhaltig bewegen. Chemical and immunohistochemical analyses have demonstrated that Aβ. and Aβ. peptides are present in vascular amyloid deposits with a preponderance of the former peptide. The accumulation of cerebrovascular amyloid leads to obliteration of capillary lumen and destruction arterial myocytes resultin作者: 清真寺 時間: 2025-3-29 18:08 作者: indicate 時間: 2025-3-29 22:33
Dennis Ahrholdt,Goetz Greve,Gregor Hopf of AD cases exhibit cerebrovascular pathology, which involves the cellular elements that represent the blood-brain barrier. However, certain vascular lesions such as microvascular degeneration affecting the cerebral endothelium, cerebral amyloid angiopathy and periventricular white matter lesions a作者: 剝皮 時間: 2025-3-30 00:14
Dennis Ahrholdt,Goetz Greve,Gregor Hopfr of other components, referred to as amyloid β-associated proteins. In this review we will discuss which proteins can be found in the cerebral vessel walls that are affected by CAA, what the possible source of these proteins is, and to what extent they might contribute to the pathogenesis of CAA. T作者: RODE 時間: 2025-3-30 05:41 作者: cardiopulmonary 時間: 2025-3-30 09:35
https://doi.org/10.1007/978-3-658-40652-3which amyloid is deposited as CAA include hereditary cerebral hemorrhage with amyloidosis of Icelandic and Dutch types, the Hungarian and Ohio kindreds of meningocerebrovascular amyloidosis and the gelsolin-related spinal and CAA. Recently, two forms of dementia associated with CAA not presenting ce作者: 滲透 時間: 2025-3-30 12:41 作者: paltry 時間: 2025-3-30 20:09
http://image.papertrans.cn/c/image/223278.jpg作者: 熱心 時間: 2025-3-31 00:07
https://doi.org/10.1007/978-94-017-1007-7Alzheimer; Grading; Lipoprotein; alzheimer‘s disease; brain; genetics; hereditary cerebral hemorrhage; mole作者: CANE 時間: 2025-3-31 01:55
978-90-481-5480-7Springer Science+Business Media Dordrecht 2000作者: conservative 時間: 2025-3-31 06:35
Clinical Aspects and Diagnostic Criteria of Sporadic CAA-Related Hemorrhage. Though fundamentally a neuropathologic diagnosis, CAA can be identified with good reliability during life by the presence on gradient-echo MRI of multiple, strictly lobar hemorrhages without other definite cause. The relatively good recovery from a first CAA-related hemorrhage is counterbalanced b作者: Dictation 時間: 2025-3-31 09:41
Diagnosis of CAA during Life These tests should be noninvasive to allow for broad and repeated application. Specific neuroimaging methods targeted at the hallmark constituent of CAA, the Aβ deposits, are particularly attractive goals. A useful technique has to be significantly more sensitive and specific than the currently ava作者: Locale 時間: 2025-3-31 16:43 作者: inconceivable 時間: 2025-3-31 20:44 作者: Irrepressible 時間: 2025-4-1 00:06
APOE Genotype in Relation to Sporadic and Alzheimer-Related CAA transport and metabolism. Following genetic linkage of late-onset familial Alzheimer’s disease to chromosome 19 and the identification of ApoE in senile plaques, neurofibrillary tangles and amyloid-laden blood vessels, over-representation of the . ε4 allele was recognized in both familial late-onse
