Transmission of pathogenic protein aggregates in Alzheimer's disease

Deposits of amyloid peptide A beta 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 A beta 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 A beta aggregates Other experiments indicate that amyloid peptide A beta 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 A beta protein can be transmitted between cells and analyzes the current evidence concerning the possibility of horizontal A beta transmission from person to person.