Secondary microvascular degeneration in amyloid angiopathy of patients with hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D)
| Autor: | H. V. Vinters, Remco Natté, Raymund A.C. Roos, Ingrid M. Hegeman-Kleinn, Corrie Welling-Graafland, Joost Haan, S. G. Van Duinen, Marion L.C. Maat-Schieman |
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| Rok vydání: | 1998 |
| Předmět: |
Pathology
medicine.medical_specialty Amyloid beta Pathology and Forensic Medicine Angiopathy Cellular and Molecular Neuroscience mental disorders medicine Humans cardiovascular diseases Fibrinoid necrosis Cerebral Hemorrhage Amyloid beta-Peptides biology business.industry Macrophages Amyloidosis Microangiopathy Brain Nuclear Proteins nutritional and metabolic diseases Antigens Nuclear Cerebral Arteries medicine.disease Capillaries Cerebral Amyloid Angiopathy Hereditary cerebral hemorrhage with amyloidosis biology.protein Neurology (clinical) Cerebral amyloid angiopathy business Biomarkers Calcification |
| Zdroj: | Acta Neuropathologica. 95:235-244 |
| ISSN: | 1432-0533 0001-6322 |
| Popis: | Various secondary microvascular degenerative and inflammatory alterations may complicate cerebral amyloid angiopathy (CAA) and contribute to the morbidity of CAA-associated stroke. We have investigated the severity of CAA-associated microangiopathy in a genetically determined Dutch form of CAA (HCHWA-D) that has major similarities to the type of CAA that more commonly occurs with aging or Alzheimer's disease (AD). The presence and extent of the following vascular abnormalities was assessed: (1) hyalinization/fibrosis, (2) microaneurysm formation, (3) chronic (especially lymphocytic) inflammation, (4) perivascular multinucleated giant cells/granulomatous angiitis, (5) macrophages/histiocytes within the vessel wall, (6) vessel wall calcification, (7) fibrinoid necrosis, and (8) mural or occlusive thrombi. (Of these, calcification of CAA-affected vessel walls has, to our knowledge, been described in only a single patient with CAA-associated cerebral hemorrhage.) Some of the changes, such as histiocytes in blood vessel walls and the relationship of vascular hyalinosis to amyloid beta/A4 protein deposition, were highlighted by immunohistochemistry. By assessing the numbers of sections in which the changes were present for each case, a 'score' reflective of CAA-associated angiopathy could be obtained. This 'score' was reproducible among several observers. We suggest that it might also be applicable to quantifying severe CAA and related microvascular degenerative changes in patients with AD. beta/A4 immunoreactivity was often sparse and adventitial (or almost absent) in severely hyalinized arterioles and microaneurysms. However, macrophages were prominent in the walls of such vessels and may play a role in the pathogenesis and progression of CAA-related microvasculopathy. |
| Databáze: | OpenAIRE |
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