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Photostimulation of extravasation of Beta-Amyloid through the model of blood-brain barrier

Urheber*innen

Zinchenko,  Ekaterina
External Organizations;

Klimova,  Maria
External Organizations;

Mamedova,  Aysel
External Organizations;

Agranovich,  Ilana
External Organizations;

Blokhina,  Inna
External Organizations;

Antonova,  Tatiana
External Organizations;

Terskov,  Andrey
External Organizations;

Shirokov,  Alexander
External Organizations;

Navolokin,  Nikita
External Organizations;

Morgun,  Andrey
External Organizations;

Osipova,  Elena
External Organizations;

Boytsova,  Elizaveta
External Organizations;

Yu,  Tingting
External Organizations;

Zhu,  Dan
External Organizations;

/persons/resource/Juergen.Kurths

Kurths,  Jürgen
Potsdam Institute for Climate Impact Research;

Semyachkina-Glushkovskaya,  Oxana
External Organizations;

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Zitation

Zinchenko, E., Klimova, M., Mamedova, A., Agranovich, I., Blokhina, I., Antonova, T., Terskov, A., Shirokov, A., Navolokin, N., Morgun, A., Osipova, E., Boytsova, E., Yu, T., Zhu, D., Kurths, J., Semyachkina-Glushkovskaya, O. (2020): Photostimulation of extravasation of Beta-Amyloid through the model of blood-brain barrier. - Electronics, 9, 6, 1056.
https://doi.org/10.3390/electronics9061056


Zitierlink: https://publications.pik-potsdam.de/pubman/item/item_24492
Zusammenfassung
Alzheimer’s disease (AD) is an incurable pathology associated with progressive decline in memory and cognition. Phototherapy might be a new promising and alternative strategy for the effective treatment of AD, and has been actively discussed over two decades. However, the mechanisms of therapeutic photostimulation (PS) effects on subjects with AD remain poorly understood. The goal of this study was to determine the mechanisms of therapeutic PS effects in beta-amyloid (Aβ)-injected mice. The neurological severity score and the new object recognition tests demonstrate that PS 9 J/cm2 attenuates the memory and neurological deficit in mice with AD. The immunohistochemical assay revealed a decrease in the level of Aβ in the brain and an increase of Aβ in the deep cervical lymph nodes obtained from mice with AD after PS. Using the in vitro model of the blood-brain barrier (BBB), we show a PS-mediated decrease in transendothelial resistance and in the expression of tight junction proteins as well an increase in the BBB permeability to Aβ. These findings suggest that a PS-mediated BBB opening and the activation of the lymphatic clearance of Aβ from the brain might be a crucial mechanism underlying therapeutic effects of PS in mice with AD. These pioneering data open new strategies in the development of non-pharmacological methods for therapy of AD and contribute to a better understanding of the PS effects on the central nervous system. View Full-Text