Autor: |
Gorina, Ya. V., Kharitonova, E. V., Khilazheva, E. D., Semenova, A. A., Morgun, A. V., Komleva, Yu. K., Lopatina, O. L., Salmina, A. B. |
Zdroj: |
Cell & Tissue Biology; Apr2023, Vol. 17 Issue 2, p105-121, 17p |
Abstrakt: |
Decreased brain energy metabolism correlates with cognitive impairment in Alzheimer's disease. There is accumulating experimental evidence that indicates that lactate transporters and monocarboxylate transporters (MCTs) are directly involved in cerebral energy metabolism. However, changes in lactate and MCT levels in Alzheimer's disease remain unclear at this time. The study aimed to investigate the content of lactate and its transporters MCT1 and MCT2 in neuronal, astroglial, and endothelial cells under acute toxic effects of β-amyloid (Aβ1–42) in vitro and in vivo. It was shown that, under conditions of acute toxic action of Aβ1–42 in vivo, the level of lactate in the hippocampal tissue significantly (p ≤ 0.05) decreased, while it increased in the dialysate against the background of low levels of MCT1 and MCT2. High production of lactate by astrocytes (p ≤ 0.05) and low level of MCT2 on neurons (p ≤ 0.05) were revealed in vitro. Thus, Aβ1–42 caused a decrease in the level of lactate in the hippocampal tissue and an increase in its level in the dialysate in vivo, which correlated with impaired levels of MCT1 and MCT2. This indicates a disorder of energy metabolism due to the acute toxic effect of Aβ1–42. At the same time, the revealed enlargement in lactate production by astrocytes in vitro may point to the triggering of a compensatory mechanism aimed at maintaining astrocytic-neuronal interaction. [ABSTRACT FROM AUTHOR] |
Databáze: |
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