摘要
Amyloid beta (A beta) peptide deposits are one of the hallmarks of Alzheimer's disease (AD). For a long time it was believed that amyloid deposits in the senile plaques in the brain of patients with AD play a central role in the etiology of AD. Later many reports ascribed this role to different aggregates of A beta (from fibrils, through high oligomers to soluble A beta oligomers) through influencing different functions of brain cells, but the results are very controversial. To study the role of A beta 1-42 as monomer and in high oligomer states we used the model of neuronal networks cultured on microelectrode arrays (MEAs) where the effect of A beta 1-42 on the electrical activity can be measured. The electrical activity of the neurons was inhibited by A beta 1-42 monomers but not by A beta 1-42 high oligomers.
The presented data support the hypothesis that it is the monomeric form of A beta which participates in the pathogenesis of AD.
- 出版日期2010