Transmission of pathogenic protein aggregates in Alzheimer’s disease. Schwarzman, A. & Sarantseva, S. Molecular Biology, 51(3):368-371, Maik Nauka Publishing / Springer SBM, 2017. cited By 2![Transmission of pathogenic protein aggregates in Alzheimer’s disease [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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. © 2017, Pleiades Publishing, Inc.
@ARTICLE{Schwarzman2017368,
author={Schwarzman, A.L. and Sarantseva, S.V.},
title={Transmission of pathogenic protein aggregates in Alzheimer’s disease},
journal={Molecular Biology},
year={2017},
volume={51},
number={3},
pages={368-371},
doi={10.1134/S0026893317030141},
note={cited By 2},
url={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85021271494&doi=10.1134%2fS0026893317030141&partnerID=40&md5=f69dbfecac3c1dec31ab554ffa036c6b},
affiliation={Konstantinov St. Petersburg Nuclear Physics Institute, Kurchatov Institute National Research Center, Gatchina, Leningrad oblast, 188300, Russian Federation},
abstract={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. © 2017, Pleiades Publishing, Inc.},
author_keywords={Alzheimer’s disease; amyloid peptide (Aβ); Aβ transmission; prions},
correspondence_address1={Schwarzman, A.L.; Konstantinov St. Petersburg Nuclear Physics Institute, Kurchatov Institute National Research CenterRussian Federation; email: aschwart1@yandex.ru},
publisher={Maik Nauka Publishing / Springer SBM},
issn={00268933},
language={English},
abbrev_source_title={Mol. Biol.},
document_type={Review},
source={Scopus},
}
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