Schwarzman A L, Sarantseva S V
Konstantinov St. Petersburg Nuclear Physics Institute Kurchatov Institute National Research Center Gatchina, Leningrad oblast Russia.
Mol Biol (Mosk). 2017 May-Jun;51(3):418-422. doi: 10.7868/S0026898417030144.
Deposits of amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein in the brain of patients are major neuropathological features of Alzheimer's disease (AD). For a long time, the possibility of horizontal transmission of Aβ aggregates from cell to cell and from person to person remained hypothetical, since there was no experimental evidence. However, in 1993, the formation of senile plaques was confirmed in the brains of animals after intracerebral injections of AD patient brain homogenates or homogenates of the brain of transgenic mice enriched with Aβ aggregates. Other experiments indicate that amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein may be transferred from cell to cell like prions. In 2015 and 2016, it was reported that AD could be transmitted to humans during medical procedures, i.e., that this disease might be iatrogenic. This review discusses the mechanisms by which pathogenic Aβ protein can be transmitted between cells and analyzes the current evidence concerning the possibility of horizontal Aβ transmission from person to person.
患者大脑中淀粉样肽Aβ的沉积和过度磷酸化tau蛋白的细胞内聚集体是阿尔茨海默病（AD）的主要神经病理学特征。长期以来，Aβ聚集体在细胞间和人际间水平传播的可能性一直只是一种假设，因为没有实验证据。然而，1993年，在向动物脑内注射AD患者脑匀浆或富含Aβ聚集体的转基因小鼠脑匀浆后，在动物大脑中证实了老年斑的形成。其他实验表明，淀粉样肽Aβ和过度磷酸化tau蛋白的细胞内聚集体可能像朊病毒一样在细胞间转移。2015年和2016年，有报道称AD可能在医疗过程中传播给人类，即这种疾病可能是医源性的。这篇综述讨论了致病性Aβ蛋白在细胞间传播的机制，并分析了目前关于Aβ在人际间水平传播可能性的证据。
