Journal of Zhejiang University SCIENCE B, Год журнала: 2024, Номер 25(6), С. 485 - 498
Опубликована: Май 15, 2024
Язык: Английский
European Journal of Medicinal Chemistry Reports, Год журнала: 2024, Номер 11, С. 100154 - 100154
Опубликована: Апрель 7, 2024
Alzheimer's disease (AD), the main dementia type accounting for over 70 % of entire population, progressive decline in memory and executive function. AD pathology is characterized by amyloid fibrils neurofibrillary tangles. Acetylcholinesterase (AChE), an enzyme involved hydrolysis neurotransmitter acetylcholine, consistently colocalizes with deposits characteristic may contribute to generation proteins. AChE a potent amyloid-promoting factor when compared other c-associated inhibitors play vital role prevent formation toxic oligomeric form peptide. Recent studies have reported that acetylcholinesterase (ChE-Is) are present plants, fungi, marine products. Some cholinesterase inhibitors, obtained from plant source such as rivastigmine, donepezil, galantamine, used treatment AD, offer alternative approach alleviate its symptoms reducing Aβ. Due limited efficacy current drugs there huge potential phytomedicines AD. Medicinal herbs herbal drug preparations traditionally been treat neurological disorders exhibiting anti-inflammatory neuroprotective properties. Phytomedicines containing flavonoids, polyphenols, naturally occurring antioxidants crosses blood-brain barrier protect neurons oxidative stress. As synthetic drugs, fewer side effects. Therefore, recent research focused explore develop it effective In our review, we summarized amyloid-deposition, Acetylcholinesterase, phytoconstituents inhibitory activity treatment.
Язык: Английский
Процитировано
26
Cells, Год журнала: 2025, Номер 14(7), С. 511 - 511
Опубликована: Март 29, 2025
Oxidative stress (OS) is an established hallmark of cancer and neurodegenerative disorders (NDDs), which contributes to genomic instability neuronal loss. This review explores the contrasting role OS in stem cells (CSCs) NDDs. Elevated levels reactive oxygen species (ROS) contribute promote tumor initiation progression CSCs, while NDDs such as Alzheimer’s Parkinson’s disease, accelerates death impairs cellular repair mechanisms. Both scenarios involve disruption delicate balance between pro-oxidant antioxidant systems, leads chronic oxidative stress. Notably, CSCs neurons display alterations redox-sensitive signaling pathways, including Nrf2 NF-κB, influence cell survival, proliferation, differentiation. Mitochondrial dynamics further illustrate these differences: enhanced function supports adaptability whereas impairments heighten vulnerability. Understanding common mechanisms OS-induced redox imbalance may provide insights for developing interventions, addressing aging hallmarks, potentially mitigating or preventing both
Язык: Английский
Процитировано
5
Scientific Reports, Год журнала: 2025, Номер 15(1)
Опубликована: Янв. 15, 2025
Язык: Английский
Процитировано
4
Molecular Neurodegeneration, Год журнала: 2025, Номер 20(1)
Опубликована: Янв. 27, 2025
Alzheimer's disease (AD) is among the most devastating neurodegenerative disorders with limited treatment options. Emerging evidence points to involvement of lipid dysregulation in development AD. Nevertheless, precise lipidomic landscape and mechanistic roles lipids pathology remain poorly understood. This review aims highlight significance lipidomics lipid-targeting approaches diagnosis We summarized connection between human brain AD at both genetic species levels. briefly introduced technologies discussed potential challenges areas future advancements field for research. To elucidate central role converging multiple pathological aspects AD, we reviewed current knowledge on interplay major features, including amyloid beta, tau, neuroinflammation. Finally, assessed progresses obstacles lipid-based therapeutics proposed strategies leveraging
Язык: Английский
Процитировано
4
Brain Research, Год журнала: 2024, Номер 1845, С. 149202 - 149202
Опубликована: Авг. 30, 2024
Язык: Английский
Процитировано
10
Journal of Neurochemistry, Год журнала: 2025, Номер 169(3)
Опубликована: Март 1, 2025
Glial cell senescence, characterized by the irreversible arrest of division and a pro-inflammatory secretory phenotype, has emerged as critical player in pathogenesis Alzheimer's disease (ad). While much attention been devoted to role neurons ad, growing evidence suggests that glial cells, including astrocytes, microglia, oligodendrocytes, contribute significantly progression through senescence. In this review, we explore molecular mechanisms underlying senescence focusing on cellular signaling pathways, DNA damage response accumulation senescence-associated phenotypes (SASP). We also examine how senescent cells exacerbate neuroinflammation, disrupt synaptic function, promote neuronal death ad. Moreover, discuss emerging therapeutic strategies aimed at targeting mitigate neurodegenerative processes By providing comprehensive overview current research disease, review highlights its potential novel target fight against
Язык: Английский
Процитировано
2
Chemical Biology & Drug Design, Год журнала: 2024, Номер 103(4)
Опубликована: Апрель 1, 2024
Abstract Neurodegenerative disorders are devastating characterized by gradual loss of neurons and cognition or mobility impairment. The common pathological features these diseases associated with the accumulation misfolded aggregation proteins. pivotal roles autophagy proteostasis in maintaining cellular health preventing proteins, which neurodegenerative like Huntington's disease (HD), Alzheimer's (AD), Parkinson's (PD). This article presents an in‐depth examination interplay between proteostasis, highlighting how processes cooperatively contribute to homeostasis prevent pathogenic protein aggregate accumulation. Furthermore, review emphasises potential therapeutic implications targeting mitigate diseases. While advancements research hold promise for developing novel treatments, also addresses challenges complexities modulating intricate pathways. Ultimately, advancing understanding underlying mechanism provides valuable insights into avenues future directions.
Язык: Английский
Процитировано
7
Ageing Research Reviews, Год журнала: 2025, Номер 106, С. 102699 - 102699
Опубликована: Фев. 20, 2025
Язык: Английский
Процитировано
1
Egyptian Liver Journal, Год журнала: 2024, Номер 14(1)
Опубликована: Ноя. 12, 2024
Abstract Background Polyploidization, a process where cells acquire additional chromosome sets, is unique characteristic of hepatocytes. This has been increasingly recognized as an adaptive mechanism for maintaining liver function during aging, period characterized by cellular senescence, DNA damage, and metabolic dysregulation. Purpose review explores the molecular mechanisms underlying hepatocyte polyploidization its potential role in promoting resilience against aging-related decline function. We assess how polyploid hepatocytes contribute to genomic stability, stress resistance, adaptation, highlighting their relevance aging. Main body Hepatocyte occurs through such cytokinesis failure endoreplication, leading binuclear or mononuclear cells. Polyploid exhibit enhanced repair capacity, which helps mitigate accumulation age-related damage. The increased gene dosage facilitates better responses, particularly oxidative genotoxic insults. Metabolic adaptations, including xenobiotic metabolism lipid regulation, further support liver’s ability maintain homeostasis Additionally, demonstrate altered epigenetic landscapes proteostasis mechanisms, contributing improved reduced susceptibility senescence. These adaptations collectively enhance structural challenges. Conclusion represents critical protective that safeguard instability, dysfunction, stress. Understanding pathways driving could pave way novel therapeutic strategies combat disorders health span. Graphical
Язык: Английский
Процитировано
4
Опубликована: Янв. 1, 2025
Процитировано
0