Neuropharmacology, Год журнала: 2024, Номер 260, С. 110133 - 110133
Опубликована: Авг. 27, 2024
Язык: Английский
Neuropharmacology, Год журнала: 2024, Номер 260, С. 110133 - 110133
Опубликована: Авг. 27, 2024
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 95, С. 102233 - 102233
Опубликована: Фев. 14, 2024
Язык: Английский
Процитировано
18Ageing Research Reviews, Год журнала: 2024, Номер 95, С. 102209 - 102209
Опубликована: Янв. 28, 2024
Язык: Английский
Процитировано
17Neuroscience, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
2Molecular and Cellular Biochemistry, Год журнала: 2023, Номер 479(4), С. 975 - 991
Опубликована: Июнь 2, 2023
Язык: Английский
Процитировано
39Autophagy, Год журнала: 2023, Номер 20(2), С. 259 - 274
Опубликована: Сен. 15, 2023
Multiple sclerosis (MS) is a chronic progressive demyelinating disease of the central nervous system (CNS) due to an increase abnormal peripherally auto-reactive T lymphocytes which elicit autoimmunity. The main pathophysiology MS myelin sheath damage by immune cells and defect in generation oligodendrocytes. Macroautophagy/autophagy critical degradation process that eliminates dysfunctional or superfluous cellular components. Autophagy has property double-edged sword it may have both beneficial detrimental effects on neuropathology. Therefore, this review illustrates protective harmful autophagy with regard disease. prevents progression reducing oxidative stress inflammatory disorders. In contrast, over-activated associated neuropathology case use inhibitors alleviate pathogenesis MS. Furthermore, provokes activation different supporting play intricate role functions modulation regulating cell proliferation related demyelination remyelination. enhances remyelination increasing activity oligodendrocytes, astrocytes. However, induces activating microglia cells. conclusion, specific autophagic activators astrocytes, dendritic (DCs), induce against
Язык: Английский
Процитировано
35Inflammopharmacology, Год журнала: 2023, Номер 31(2), С. 673 - 688
Опубликована: Март 24, 2023
Язык: Английский
Процитировано
27Molecular Neurobiology, Год журнала: 2023, Номер 61(5), С. 2469 - 2480
Опубликована: Окт. 28, 2023
Язык: Английский
Процитировано
26Journal of Cellular and Molecular Medicine, Год журнала: 2024, Номер 28(10)
Опубликована: Май 1, 2024
Parkinson's disease (PD) is a neurodegenerative disorder of the brain and manifested by motor non-motor symptoms because degenerative changes in dopaminergic neurons substantia nigra. PD neuropathology associated with mitochondrial dysfunction, oxidative damage apoptosis. Thus, modulation apoptosis growth factors could be novel boulevard management PD. Brain-derived neurotrophic factor (BDNF) its receptor tropomyosin kinase type B (TrkB) are chiefly involved neuropathology. BDNF promotes survival nigra enhances functional activity striatal neurons. Deficiency TrkB triggers degeneration accumulation α-Syn As well, BDNF/TrkB signalling reduced early phase Targeting specific activators may attenuate this review aimed to discuss potential role against In conclusion, decreased linked severity long-term complications. Activation
Язык: Английский
Процитировано
15European journal of medical research, Год журнала: 2024, Номер 29(1)
Опубликована: Март 27, 2024
Abstract Parkinson's disease (PD) is a progressive neurodegenerative as result of the degeneration dopaminergic neurons in substantia nigra pars compacta (SNpc). The fundamental features PD are motor and non-motor symptoms. symptoms develop due to disruption neurotransmitters other such γ-aminobutyric acid (GABA). potential role GABA neuropathology concerning was not precisely discussed. Therefore, this review intended illustrate possible regarding pathway essential regulating inhibitory tone prevent excessive stimulation cerebral cortex. Degeneration linked with reducing GABAergic neurotransmission. Decreasing activity promotes mitochondrial dysfunction oxidative stress, which highly related neuropathology. Hence, restoring by agonists may attenuate progression dysregulation SNpc contributes developing Besides, also pathway, amelioration reduce In conclusion, deregulation might be intricate Improving novel, beneficial approach control
Язык: Английский
Процитировано
14Cells, Год журнала: 2024, Номер 13(2), С. 123 - 123
Опубликована: Янв. 9, 2024
The COVID-19 pandemic has brought to the forefront intricate relationship between SARS-CoV-2 and its impact on neurological complications, including potential links neurodegenerative processes, characterized by a dysfunction of protein quality control systems ER stress. This review article explores role systems, such as Unfolded Protein Response (UPR), Endoplasmic Reticulum-Associated Degradation (ERAD), Ubiquitin–Proteasome System (UPS), autophagy molecular chaperones, in infection. Our hypothesis suggests that produces stress exploits leading disruption proteostasis cannot be solved host cell. culminates cell death may represent link neurodegeneration.
Язык: Английский
Процитировано
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