Open AccessRising of intracellular NAD+ level and oppositely directed changes in CD38 expression in hippocampal cells in experimental Alzheimer’s disease
Author(s) -
А. А. Семенова,
Yana V. Gorina,
Е. Д. Хилажева,
Elena P. Kharitonova,
А. Б. Салмина
Publication year - 2021
Publication title -
sibirskij naučnyj medicinskij žurnal
Language(s) - English
Resource type - Journals
eISSN - 2410-2520
pISSN - 2410-2512
DOI - 10.18699/ssmj20210505
Subject(s) - cd38 , nad+ kinase , hippocampal formation , cyclase , extracellular , intracellular , hippocampus , medicine , endocrinology , chemistry , biology , biochemistry , enzyme , microbiology and biotechnology , stem cell , cd34
The aim of the study was to assess the level of NAD + in the brain of mice treated with beta-amyloid (Aβ), as well as to determine the activity of ADP-ribosyl cyclase/CD38 and the number of CD38-immunopositive neurons, astrocytes and endothelial cells. Material and methods. The Alzheimer’s disease model was reproduced by intrahippocampal administration of Aβ to C57BL/6 mice. Determination of the NAD + level in the extracellular fluid of the brain and in the hippocampal tissue was carried out by spectrophotometric analysis. Evaluation of the enzymatic activity of ADP-ribosyl cyclase / CD38 was carried out by the fluorimetric method, determination of the number of CD38-immunopositive cells by the immunohistochemistry method. Results and discussion. The level of NAD + was significantly increased in the hippocampal tissue in mice after administration of Aβ, while the level of extracellular NAD + did not change. The activity of ADP-ribosyl cyclase / CD38 in the hippocampal tissue did not change, but the number of CD38-immunopositive neurons decreased, and the number of CD38 + endothelial cells increased in the hippocampus of mice after administration of Aβ. Conclusion. Opposite changes in the expression of ADP-ribosyl cyclase / CD38 in neurons and endotheliocytes correspond to different metabolic states of these types of cells and, along with an increased intracellular pool of NAD + in experimental Alzheimer’s disease, reflect an adaptive stress response to Aβ administration.