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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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樓主: Aggrief
51#
發(fā)表于 2025-3-30 09:35:13 | 只看該作者
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
52#
發(fā)表于 2025-3-30 12:41:40 | 只看該作者
53#
發(fā)表于 2025-3-30 20:09:11 | 只看該作者
http://image.papertrans.cn/c/image/223278.jpg
54#
發(fā)表于 2025-3-31 00:07:56 | 只看該作者
https://doi.org/10.1007/978-94-017-1007-7Alzheimer; Grading; Lipoprotein; alzheimer‘s disease; brain; genetics; hereditary cerebral hemorrhage; mole
55#
發(fā)表于 2025-3-31 01:55:43 | 只看該作者
978-90-481-5480-7Springer Science+Business Media Dordrecht 2000
56#
發(fā)表于 2025-3-31 06:35:39 | 只看該作者
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
57#
發(fā)表于 2025-3-31 09:41:01 | 只看該作者
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
58#
發(fā)表于 2025-3-31 16:43:20 | 只看該作者
59#
發(fā)表于 2025-3-31 20:44:17 | 只看該作者
60#
發(fā)表于 2025-4-1 00:06:04 | 只看該作者
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
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