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In the present study, in modeling the pathogenesis of Alzheimer’s disease in 5xFAD transgenic mice, a comparative analysis of structural and ultrastructural changes in the nervous tissue of the olfactory bulbs, hippocampus, and entorhinal cortex was performed; in addition, the distribution of the main amyloid-degrading neuropeptidase, neprilysin (NEP), relative to wild-type mice was examined. The investigation of the structure of the nervous tissue showed that the death of brain neurons increased in transgenic animals characterized by increased production of the amyloid peptide Aβ. As a result, connections between neurons were interrupted and the neural network become disrupted. Our electron-microscopy examination revealed a reduced density of synaptic contacts and dendritic spines, local lesions of the nervous tissue, and the appearance of autophagolysosomes in the neuropil tissue of these structures in 5xFAD mice. Signs indicating increased neurodegenerative processes compared with wild-type mice were visible. In 5xFAD mice, the distribution of amyloid-degrading peptidase NEP in the entorhinal cortex and hippocampus was altered, and there was a decreased intensity of its staining in the entorhinal cortex. In transgenic mice aged 6 months, memory impairment was observed in the recognition test of new objects relative to wild-type mice.
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Tumanova et al. (2022) studied this question.
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