
Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)
Published: Oct. 24, 2024
Language: Английский
Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)
Published: Oct. 24, 2024
Language: Английский
Frontiers in Molecular Neuroscience, Journal Year: 2024, Volume and Issue: 17
Published: June 19, 2024
Cognitive impairment (COI) is a prevalent complication across spectrum of brain disorders, underpinned by intricate mechanisms yet to be fully elucidated. Neurons, the principal cell population nervous system, orchestrate cognitive processes and govern balance. Extensive inquiry has spotlighted involvement Foxo3a in COI. The regulatory cascade transactivation implicates multiple downstream signaling pathways encompassing mitochondrial function, oxidative stress, autophagy, apoptosis, collectively affecting neuronal activity. Notably, expression activity profile are subject modulation via various modalities, including methylation promoter, phosphorylation acetylation protein. Furthermore, upstream such as PI3K/AKT, SIRT family, diverse micro-RNAs intricately interface with Foxo3a, engendering alterations function. Through several routes, regulates dynamics, thereby modulating onset or amelioration COI Alzheimer’s disease, stroke, ischemic injury, Parkinson’s traumatic injury. potential therapeutic target, clinical drugs small molecules have been preliminarily shown cognitive-enhancing effects that indirectly affect Foxo3a. Particularly noteworthy randomized, controlled, placebo trials illustrating significant enhancement achievable through autophagy modulation. Here, we discussed role neuron-mediated common cognitively impaired diseases.
Language: Английский
Citations
5Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: May 2, 2025
Language: Английский
Citations
0Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown
Published: March 27, 2024
Abstract Alzheimer's disease (AD) is a progressive neurodegenerative brain disease. At present, the main treatment strategy to alleviate certain symptoms, but potential mechanisms of AD are not fully understood, and there lack effective methods in clinical practice. Quercetin (QT) can significantly protect neurodegeneration by inhibiting oxidative stress inflammation, has play greater role Therefore, this study aims explore mechanism QT based on AMPK/mTOR pathway improving learning memory abilities rats.For purpose,we established an rat model injecting Hcy into tail vein.After successful validation, AMPK inhibitor were gavaged.Then, protected nerve regeneration was determined using Morris water maze, Nissl staining, Western blot immunohistochemistry.We observed that improved models with AD, as demonstrated short latency times travel across platform. staining showed could reduce neurological Apoptosis amenorrate implementation .Western immunohistochemistry questionnaire increased p-AMPK, while reducing p-mTOR p-Tau .In addition, application specific effectively reverse these changes, further enhancing improvement effect inhibition Thereby induced rates, thus abilities.
Language: Английский
Citations
0Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)
Published: Oct. 24, 2024
Language: Английский
Citations
0