
Seizure, Journal Year: 2024, Volume and Issue: 117, P. 133 - 141
Published: Feb. 23, 2024
Language: Английский
Seizure, Journal Year: 2024, Volume and Issue: 117, P. 133 - 141
Published: Feb. 23, 2024
Language: Английский
Cellular and Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 43(6), P. 2437 - 2458
Published: Feb. 8, 2023
Language: Английский
Citations
131Journal of Environmental Sciences, Journal Year: 2022, Volume and Issue: 127, P. 589 - 602
Published: June 18, 2022
Language: Английский
Citations
73Biomedicines, Journal Year: 2023, Volume and Issue: 11(9), P. 2488 - 2488
Published: Sept. 7, 2023
Mitochondria play a vital role in maintaining cellular energy homeostasis, regulating apoptosis, and controlling redox signaling. Dysfunction of mitochondria has been implicated the pathogenesis various brain diseases, including neurodegenerative disorders, stroke, psychiatric illnesses. This review paper provides comprehensive overview intricate relationship between disease, focusing on underlying pathological mechanisms exploring potential therapeutic opportunities. The covers key topics such as mitochondrial DNA mutations, impaired oxidative phosphorylation, dynamics, calcium dysregulation, reactive oxygen species generation context disease. Additionally, it discusses emerging strategies targeting dysfunction, protective agents, metabolic modulators, gene therapy approaches. By critically analysing existing literature recent advancements, this aims to enhance our understanding multifaceted disease shed light novel interventions.
Language: Английский
Citations
66Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(8), P. 5541 - 5571
Published: Jan. 11, 2024
Language: Английский
Citations
19Biomedicines, Journal Year: 2024, Volume and Issue: 12(5), P. 1083 - 1083
Published: May 13, 2024
Welcome to
Language: Английский
Citations
17Biomolecules, Journal Year: 2020, Volume and Issue: 10(8), P. 1158 - 1158
Published: Aug. 7, 2020
Neurodegenerative diseases are the second most common cause of death and characterized by progressive impairments in movement or mental functioning central peripheral nervous system. The prevention neurodegenerative disorders has become an emerging public health challenge for our society. Melatonin, a pineal hormone, various physiological functions brain, including regulating circadian rhythms, clearing free radicals, inhibiting biomolecular oxidation, suppressing neuroinflammation. Cumulative evidence indicates that melatonin wide range neuroprotective roles pathophysiological mechanisms signaling pathways. Moreover, levels decreased patients with diseases. In this review, we summarize current knowledge on regulation, molecular biological such as Alzheimer’s disease, Parkinson’s Huntington’s amyotrophic lateral sclerosis, vascular dementia multiple sclerosis. We also discuss clinical application disorders. This information will lead to better understanding regulation brain provide therapeutic options treatment
Language: Английский
Citations
108Food Chemistry, Journal Year: 2021, Volume and Issue: 357, P. 129791 - 129791
Published: April 20, 2021
Language: Английский
Citations
96Inflammopharmacology, Journal Year: 2022, Volume and Issue: 30(5), P. 1569 - 1596
Published: June 5, 2022
Language: Английский
Citations
57Neurochemical Research, Journal Year: 2022, Volume and Issue: 47(10), P. 2909 - 2924
Published: June 11, 2022
Language: Английский
Citations
43Translational Neurodegeneration, Journal Year: 2022, Volume and Issue: 11(1)
Published: May 9, 2022
Abstract Background Intracellular accumulation of the microtubule-associated protein tau and its hyperphosphorylated forms is a key neuropathological feature Alzheimer’s disease (AD). Melatonin has been shown to prevent hyperphosphorylation in cellular animal models. However, molecular mechanisms by which melatonin attenuates tau-related pathologies are not fully understood. Methods Immunofluorescence, immunoblotting analysis thioflavin-S staining were employed examine effects early late treatment on pathology hTau mice, nonmutated human overexpressed mouse knockout background. High-throughput microRNA (miRNA) sequencing, quantitative RT-PCR, luciferase reporter assay performed determine mechanism. Results We found that both efficiently decreased phosphorylation soluble insoluble at sites related AD. Moreover, significantly reduced number neurofibrillary tangles (NFTs) attenuated neuronal loss cortex hippocampus. Furthermore, using miRNA microarray analysis, we miR-504-3p expression was upregulated mice. The administration mimics dramatically targeting p39, an activator well-known kinase cyclin-dependent 5 (CDK5). Compared with alone, co-treatment p39 failed reduce hyperphosphorylation. Conclusions Our results suggest for first time alleviates through upregulation p39/CDK5 axis provide novel insights into AD strategies.
Language: Английский
Citations
38