Опубликована: Янв. 1, 2024
Язык: Английский
Опубликована: Янв. 1, 2024
Язык: Английский
Experimental Neurology, Год журнала: 2025, Номер 386, С. 115151 - 115151
Опубликована: Янв. 19, 2025
Язык: Английский
Процитировано
0Brain Research Bulletin, Год журнала: 2025, Номер 222, С. 111245 - 111245
Опубликована: Фев. 7, 2025
Mitochondrial dysfunction and neuronal impairment are hallmark features of Diabetes-Associated Cognitive Dysfunction (DACD), mitochondrial transplantation is also a therapeutic intervention for DACD. However, the precise mechanism underlying its effects not fully elucidated. Given that imbalances in copper homeostasis cuproptosis associated with various neurodegenerative disorders diabetic myocardial damage, we hypothesize role pathogenesis We further propose peripheral may ameliorate DACD by reducing processes cuproptosis. In this research, study delved into expression levels cuproptosis-associated proteins FDX1, LIAS, DLAT, as well content both type 2 diabetes mellitus (T2DM) mice primary cells exposed to high glucose palmitic acid (HG/Pal). Furthermore, cognitive capabilities were evaluated using series behavioral tests. The findings revealed neurons HG/Pal, was elevated, DLAT reduced. Post-transplantation platelet-derived mitochondria (Mito-Plt), significant reversal these biomarkers noted, coincident an improvement deficits T2DM mice. Significantly, agonist elesclomol (ES) aggravated alterations. summary, collectively suggest causal connection between development neurons. use exogenous Mito-Plt presents promising approach, capable rescuing from thereby potentially alleviating
Язык: Английский
Процитировано
0Behavioural Brain Research, Год журнала: 2025, Номер unknown, С. 115493 - 115493
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0Neuropsychopharmacology, Год журнала: 2024, Номер unknown
Опубликована: Ноя. 7, 2024
Язык: Английский
Процитировано
2Neurochemical Research, Год журнала: 2024, Номер 50(1)
Опубликована: Ноя. 18, 2024
Язык: Английский
Процитировано
0Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
0