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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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楼主: Aggrief
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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.
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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.
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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.
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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
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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.
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