Autoimmune responses to amyloid structures of Abeta(25-35) peptide and human lysozyme in the serum of patients with progressive Alzheimer's disease
| Autor: | M A, Gruden, T B, Davudova, M, Malisauskas, V V, Zamotin, R D E, Sewell, N I, Voskresenskaya, I A, Kostanyan, V V, Sherstnev, L A, Morozova-Roche |
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| Rok vydání: | 2004 |
| Předmět: |
Amyloid
Amyloid beta-Peptides Brain Immunoglobulins Enzyme-Linked Immunosorbent Assay Antigen-Antibody Complex Microscopy Atomic Force Magnetic Resonance Imaging Peptide Fragments Diagnosis Differential Cerebral Amyloid Angiopathy Alzheimer Disease Reference Values Disease Progression Humans Immune Complex Diseases Female Muramidase Mental Status Schedule Tomography X-Ray Computed Aged Autoantibodies |
| Zdroj: | Dementia and geriatric cognitive disorders. 18(2) |
| ISSN: | 1420-8008 |
| Popis: | We have found an increased level of serum antibodies to the prefibrillar structures of both Abeta(25-35) peptide and human lysozyme in Alzheimer's disease (AD) patients compared to age-matched controls, indicating that autoimmunity is implicated in AD. In the serum of AD patients with a long-term duration (15 years) the titer of serum antibodies to aggregates of Abeta(25-35) peptide increased by approximately 5-fold, whilst the antibody titer to lysozyme protofilaments decreased by approximately 8-fold compared to patients with AD duration of5 years. The content of immunoglobulins of the A, G and M types declined, particularly in AD duration of15 years. An increase in the concentration of immune complexes and higher lysozyme activity was detected in the serum of all patients and this was suggestive of an inflammatory reaction. We propose that the autoimmune response to different amyloid structures in AD can be viewed as a clearance pathway targeting amyloid development. Autoimmune response can be exploited as a marker of ongoing protein aggregation and hence be used as a diagnostic feature of AD. |
| Databáze: | OpenAIRE |
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