Inoculation of mice with brain homogenates from patients with sporadic Alzheimer's disease can cause brain amyloid to deposit in the recipients. This suggests that β-amyloid (Aβ) peptide may self-pro

  Inoculation of mice with brain homogenate from patients with sporadic Alzheimer's disease can cause brain amyloid to deposit in the recipient. This suggests that the β-amyloid (Aβ) peptide may self-proliferate as a prion.

  Stanley Prussiner et al. tested whether the brain was inoculated with two synthetic β-amyloid (Aβ) peptides (composed of 40 or 42 amino acids and aggregated into amyloid fibrils). Plaque formation causes plaque, which is characteristic of Alzheimer's disease. The authors found that this synthetic β-amyloid (Aβ) peptide 40 preparation composed of long and thin fibrils filled the corpus callosum, hippocampus, and cerebral cortex of recipient mice with these two peptides. The preparation of β-amyloid (Aβ) peptide 42 composed of short fibrils caused a smaller number of plaques, mainly containing β-amyloid (Aβ) peptide 42, however, use a low concentration of detergent before inoculation SDS treatment of these amyloid preparations can eliminate the observed differences in plaque content, number, and distribution. The author believes that the type of amyloid β (Aβ) that may cause pathological heterogeneity in patients with Alzheimer's disease may contribute to the increase in the treatment grade of patients. exist

  In a related study, Prusiner and his colleagues tested whether different amyloid β (Aβ) aggregates are distributed in the brains of different Alzheimer's disease patients. This can complicate drug development. When the author inoculated transgenic mice with brain homogenates from two patients with different hereditary Alzheimer's disease—the Arctic mutations in these patients rearranged these β-amyloid (Aβ) peptides...or appeared in Swedish mutations outside of these sequences-various patterns and abundant amyloid deposits appear in the brain. In addition, if these β-amyloid (Aβ) types continue to grow in mice, these differences will persist. This indicates that these types of prion-like transmissibility. The author found that monoclonal antibodies developed against certain types of beta amyloid (Aβ) for passive Alzheimer’s disease immunotherapy may not be effective against other types. In the past, he said this led to a series of types of methods. fail.