Complement Activation in Very Early Alzheimer Disease
| Autor: | Caleb E. Finch, H. Zanjani, Joseph L. Price, Daniel W. McKeel, Claudia Kemper, John P. Atkinson, John C. Morris |
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| Rok vydání: | 2005 |
| Předmět: |
Male
Pathology medicine.medical_specialty Amyloid Clinical Dementia Rating chemical and pharmacologic phenomena Degenerative disease Alzheimer Disease mental disorders medicine Humans Dementia Senile plaques Aged Aged 80 and over Analysis of Variance Amyloid beta-Peptides Clusterin biology business.industry Complement System Proteins Middle Aged medicine.disease Complement system Psychiatry and Mental health Clinical Psychology biology.protein Female Geriatrics and Gerontology Alzheimer's disease business Gerontology |
| Zdroj: | Alzheimer Disease & Associated Disorders. 19:55-66 |
| ISSN: | 0893-0341 |
| DOI: | 10.1097/01.wad.0000165506.60370.94 |
| Popis: | The activation of the classical complement (C)-system in early-stage Alzheimer disease (AD) and nondemented aging was examined with immunohistochemistry in subjects assessed by the Clinical Dementia Rating (CDR). Activation (staining for C3 and C4 fragments) was found in all brains with amyloid deposits, including all nondemented (CDR 0) cases, with either small numbers of diffuse plaques or with sufficient plaques and tangles to indicate preclinical AD. Staining for C3 and C4 increased in parallel with plaque density in very mild to severe clinical AD. A subset of very mild AD (CDR 0.5) cases also showed C1q (on plaques) and C5b-9 (on neuritic plaques and tangles), whereas these C-fragments were consistently found in severe AD (CDR 3). Mirror section (split-face) analysis showed that C1q, C3, and apoJ (clusterin) occurred on the same plaques. However, C-system regulators CD59, CR1, DAF, and MCP were not detected on plaques or tangles at any stage, indicating that C-activation related to AD is incompletely controlled. |
| Databáze: | OpenAIRE |
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