Comparison of Morphological Signs of Neurodegenerative Changes and Expression of Neuroprotective Factors in Adult and Aged Wistar Rats in AlCl3-Induced Neurodegeneration

Aluminum ions are an immunostimulating agent and a promoter of the production of ROS that play a key role in the pathogenesis of age-related diseases. The severity of morphological signs of neurodegeneration caused by chronic intake of AlCl3 aqueous solution (100 mg/kg, 60 days) and mRNA expression of genes encoding the neuroprotective factor BDNF and the antioxidant enzyme GPX4 were compared in adult and aged male Wistar rats. In comparison with the adult control rats, aged animals showed a more pronounced immunohistochemical reaction with antibodies to tau protein (pTau) in the entorhinal and temporal cortex. In adult animals of the experimental group, a significant increase in the aluminum level in the hippocampus and temporal cortex was observed, which was accompanied by enhanced Gpx4 mRNA expression. In aged rats of the experimental group, no significant accumulation of aluminum in the brain was observed in comparison with the corresponding control, while the expression of Bdnf and Gpx4 was markedly reduced and the content of intracellular amyloid fibrils and pTau+ inclusions in neurons, mainly localized in the entorhinal and temporal regions, was higher. The obtained data complement previous studies and confirm the high relevance of this model for further study of the mechanisms of initiation and progression of neurodegenerative processes in humans. © Springer Science+Business Media, LLC, part of Springer Nature 2026.

Издательство
New York Consultants BureauSpringer / Автономная некоммерческая организация Издательство Российской академии медицинских наук
Номер выпуска
6
Язык
Английский
Страницы
778-784
Статус
Опубликовано
Том
179
Год
2025
Организации
  • 1 Petrovsky National Research Centre of Surgery, Moscow, Russian Federation
  • 2 RUDN University, Moscow, Moscow Oblast, Russian Federation
Ключевые слова
aging; hyperphosphorylated tau; neurodegeneration; oxidative stress; β-amyloid
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