Changes in the Number of CD38 and CX43 Immunopositive Cells in the Neurovascular Unit of the Brain in Experimental Alzheimer’s Disease

It is known that mitochondrial dysfunction can be a trigger or a concomitant mechanism in the development of Alzheimer’s disease. It is also known that the restoration of intracellular mitochondrial activity of neurons and cerebral endotheliocytes is possible due to the transfer of intact mitochondr...

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Bibliographic Details
Published in:Cell and tissue biology 2022-04, Vol.16 (2), p.121-129
Main Authors: Khilazheva, E. D., Mosyagina, A. I., Morgun, A. V., Malinovskaya, N. A., Gorina, Ya. V., Kharitonova, E. V., Lopatina, O. L., Salmina, A. B.
Format: Article
Language:English
Subjects:
Alzheimer's disease
Astrocytes
Biomedical and Life Sciences
Blood-brain barrier
Brain
CD38 antigen
Cell Biology
Connexin 43
Life Sciences
Mitochondria
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
Permeability
β-Amyloid
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Summary:It is known that mitochondrial dysfunction can be a trigger or a concomitant mechanism in the development of Alzheimer’s disease. It is also known that the restoration of intracellular mitochondrial activity of neurons and cerebral endotheliocytes is possible due to the transfer of intact mitochondria from other brain cells—in particular, astrocytes—and this transfer of mitochondria is mediated by the CD38 protein and functionally linked to it connexin 43 (Cx43). It follows that these molecules are promising for study both in relation to the mechanisms of development of neurodegeneration and in relation to the possible modulation of their activity for the correction of neurological deficits. The aim of this work was to study changes in the number of CD38- and Cx43-immunopositive cells in the neurovascular unit and the blood–brain barrier (BBB) of the brain in experimental Alzheimer’s disease. We have shown that the toxic effect of β-amyloid leads to a significant increase in the number of CD38- and Cx43-positive cells as in the hippocampus of animals in vivo, and as part of the BBB model in vitro. We have also shown that the cultivation of isolated astrocytes in the presence of β-amyloid leads to an increase in the content of Cx43 in cells and that the permeability of these half-channels significantly increases.
ISSN:1990-519X
1990-5203
DOI:10.1134/S1990519X22020067