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Titlebook: Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders; Marcel M. Verbeek,Robert M. W. Waal,Harry V. Vinte Book 2000 Spr

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書目名稱Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders
編輯Marcel M. Verbeek,Robert M. W. Waal,Harry V. Vinte
視頻videohttp://file.papertrans.cn/224/223278/223278.mp4
圖書封面Titlebook: Cerebral Amyloid Angiopathy in Alzheimer’s Disease and Related Disorders;  Marcel M. Verbeek,Robert M. W. Waal,Harry V. Vinte Book 2000 Spr
描述Cerebral amyloid angiopathy (CAA) is a distinctive abnormalityof small cerebral blood vessels, one that has intriguedneuroscientists for decades. The time 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 systemsbe used to understand the etiology of, or even potential treatmentsfor, CAA? The editors have assembled key figures in the field of CAAresearch to examine these (and other) questions in a series of focusedchapters that address specific issues of importance in understandingCAA and its clinical manifestations. Comprehending the biology andpathogenesis of this fascinating vascular lesion may even provideclues to less common forms of cerebral microvascular disease that havebeen recognized for decades (hypertensive microangiopathy) or morerecently (CADASIL).
出版日期Book 2000
關(guān)鍵詞Alzheimer; Grading; Lipoprotein; alzheimer‘s disease; brain; genetics; hereditary cerebral hemorrhage; mole
版次1
doihttps://doi.org/10.1007/978-94-017-1007-7
isbn_softcover978-90-481-5480-7
isbn_ebook978-94-017-1007-7
copyrightSpringer Science+Business Media Dordrecht 2000
The information of publication is updating

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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.
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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.
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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.
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