Immunological Approach for the Treatment of Alzheimer's Disease
| Autor: | Beka Solomon |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Genetically modified mouse
Amyloid Amyloid beta medicine.drug_class Mice Transgenic Plaque Amyloid Monoclonal antibody Epitope Epitopes Mice Cellular and Molecular Neuroscience Alzheimer Disease Antibody Specificity mental disorders medicine Animals Memory Disorders Amyloid beta-Peptides biology P3 peptide Antibodies Monoclonal Brain General Medicine medicine.disease Molecular biology Peptide Fragments Protein Structure Tertiary Disease Models Animal biology.protein Alzheimer's disease Antibody |
| Zdroj: | Journal of Molecular Neuroscience. 20:283-286 |
| ISSN: | 0895-8696 |
| Popis: | Formation of amyloid beta (Abeta) is a complex kinetic and thermodynamic process, dependent on peptidepeptide interactions that may be modulated by other proteins. We found that site-directed antibodies toward peptide (glutamic acid, phenyl alanine, arginine, histidine) EFRH sequences 3-6 of the N-terminal region of beta-amyloid peptide (AbetaP) suppress in vitro formation of Abeta and dissolve already formed fibrillar amyloid. These so-called chaperone-like properties of monoclonal antibodies led to the development of a new immunological approach toward Alzheimer's disease (AD) treatment. Production and performance of anti-Abeta antibodies into the transgenic mouse model of AD showed that these antibodies may be delivered from the periphery to the central nervous system, preventing the formation of Abeta and dissolving amyloid plaques. Moreover, immunization with Abeta protects transgenic mice from the learning and age-related memory deficits that occur in AD. These data support the hypotheses that AbetaP plays a central role in AD, and site-directed antibodies that modulate AbetaP conformation might lead toward immunotherapy of the disease. |
| Databáze: | OpenAIRE |
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