| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2010-08-18 |
| タイトル |
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|
タイトル |
＜Symposium IV＞Cerebral amyloid angiopathy and Alzheimer's disease |
| 言語 |
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|
言語 |
eng |
| 資源タイプ |
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|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 著者 |
Ghiso, Jorge
Tomidokoro, Yasushi
Revez, Tamas
Frangione, Blas
Rostagno, Agueda
|
| 著者所属 |
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|
値 |
Department of Pathology, New York University School of Medicine |
| 著者所属 |
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|
値 |
Department of Clinical Sciences, Tsukuba University |
| 著者所属 |
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|
値 |
Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, University College London |
| 著者所属 |
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|
値 |
Department of Pathology, New York University School of Medicine |
| 著者所属 |
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|
値 |
Department of Pathology, New York University School of Medicine |
| 抄録 |
|
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内容記述タイプ |
Abstract |
|
内容記述 |
Cerebral amyloid angiopathy （CAA） is increasingly recognized as a major contributor of Alzheimer’s disease（ AD） pathogenesis. To date, vascular deposits and not parenchymal plaques appear more sensitive predictors of dementia. Amyloid deposition in and around cerebral blood vessels plays a central role in a series of response mechanisms that lead to changes in the integrity of the blood-brain barrier, extravasations of plasma proteins, edema formation, release of inflammatory mediators and matrix metalloproteases which, in turn, produce partial degradation of the basal lamina with the potential to develop hemorrhagic complications. The progressive buildup of amyloid deposits in and around blood vessels chronically limits blood supply and causes focal deprivation of oxygen, triggering a secondary cascade of metabolic events several of which involve the generation of nitrogen and oxygen free radicals with consequent oxidative stress and cell toxicity. Many aspects of CAA in early- and lateonset AD ‒the special preference of Aβ40 to deposit in the vessel walls, the favored vascular compromise associated with many Aβ genetic variants, the puzzling observation that some of these vasculotropic variants solely manifest with recurrent hemorrhagic episodes while others are mainly associated with dementia‒ await clarifi cation. Non-Aβ cerebral amyloidoses reinforce the viewpoint that plaque burden is not indicative of dementia while highlighting the relevance of non-fi brillar lesions and vascular involvement in the disease pathogenesis. The lessons learned from the comparative study of Aβ and non-Aβ cerebral amyloidosis provide new avenues and alternative models to study the role of amyloid in the molecular basis of neurodegeneration. |
| 引用 |
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内容記述タイプ |
Other |
|
内容記述 |
弘前医学. 61(Suppl.), 2010, p.S111-S124 |
| 書誌情報 |
弘前医学
巻 61,
号 Supplement,
p. S111-S124,
発行日 2010-07-08
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| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
0439-1721 |
| 書誌レコードID |
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収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00211444 |
| 著者版フラグ |
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出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 日本十進分類法 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| NIIサブジェクト |
|
|
主題Scheme |
Other |
|
主題 |
医学 |
| 出版者 |
|
|
出版者 |
弘前大学大学院医学研究科・弘前医学会 |
| 資源タイプ |
|
|
値 |
Article |
HirosakiMedJ_61_S111.pdf (293.3 kB)
