Life Sciences, Journal Year: 2024, Volume and Issue: 359, P. 123225 - 123225
Published: Nov. 9, 2024
Language: Английский
Life Sciences, Journal Year: 2024, Volume and Issue: 359, P. 123225 - 123225
Published: Nov. 9, 2024
Language: Английский
European journal of medical research, Journal Year: 2024, Volume and Issue: 29(1)
Published: March 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
Language: Английский
Citations
16Autophagy, Journal Year: 2024, Volume and Issue: 20(7), P. 1473 - 1482
Published: Feb. 12, 2024
Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ) that results from autoantibodies against nicotinic acetylcholine receptors (nAchRs) at NMJs. These are mainly originated autoreactive B cells bind and destroy nAchRs NMJs preventing nerve impulses activating end-plates skeletal muscle. Indeed, immune dysregulation plays a crucial role in pathogenesis MG. Autoreactive increased MG due to defect central peripheral tolerance mechanisms. As well, T augmented diversion regulatory (T
Language: Английский
Citations
13Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(9), P. 7092 - 7108
Published: Feb. 17, 2024
Abstract Parkinson’s disease (PD) is a progressive neurodegenerative of the brain due to degeneration dopaminergic neurons in substantia nigra (SN). Glycogen synthase kinase 3 beta (GSK-3β) implicated pathogenesis PD. Therefore, purpose present review was revise mechanistic role GSK-3β PD neuropathology, and how inhibitors affect neuropathology. GSK-3 conserved threonine/serine protein that intricate regulation cellular anabolic catabolic pathways by modulating glycogen synthase. Over-expression also interconnected with development different diseases. However, underlying mechanism neuropathology not fully clarified. induces triggering mitochondrial dysfunction oxidative stress SN. NF-κB NLRP3 inflammasome are activated response dysregulated leading neuronal injury. Higher expression early stages might contribute reduction neuroprotective brain-derived neurotrophic factor (BDNF). Thus, may be effective reducing inflammatory disorders which associated
Language: Английский
Citations
12European journal of medical research, Journal Year: 2024, Volume and Issue: 29(1)
Published: Feb. 9, 2024
Abstract Multiple sclerosis (MS) is the most frequent inflammatory and demyelinating disease of central nervous system (CNS). The underlying pathophysiology MS destruction myelin sheath by immune cells. formation plaques, inflammation, injury neuronal characterizes its neuropathology. plaques are multiple focal regions demyelination disseminated in brain's white matter, spinal cords, deep grey cerebral cortex. Fenofibrate a peroxisome proliferative activated receptor alpha (PPAR-α) that attenuates reactions MS. inhibits differentiation Th17 inhibiting expression pro-inflammatory signaling. According to these findings, this review intended illuminate mechanistic immunoinflammatory role fenofibrate mitigating In conclusion, can attenuate neuropathology modulating different pathways, including oxidative stress, autophagy, mitochondrial dysfunction, inflammatory-signaling neuroinflammation.
Language: Английский
Citations
11Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 94, P. 102200 - 102200
Published: Jan. 17, 2024
Language: Английский
Citations
10Life Sciences, Journal Year: 2024, Volume and Issue: 357, P. 123088 - 123088
Published: Sept. 30, 2024
Language: Английский
Citations
6European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 177419 - 177419
Published: Feb. 1, 2025
Language: Английский
Citations
0Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0Brain Research Bulletin, Journal Year: 2025, Volume and Issue: unknown, P. 111349 - 111349
Published: April 1, 2025
Language: Английский
Citations
0Journal of Alzheimer s Disease, Journal Year: 2024, Volume and Issue: 99(4), P. 1261 - 1271
Published: May 23, 2024
Background: Reliable blood biomarkers are crucial for early detection and treatment evaluation of cognitive impairment, including Alzheimer’s disease other dementias. Objective: To examine whether plasma their combination different between older people with mild impairment (MCI) cognitively normal individuals, to explore relations performance. Methods: This cross-sectional study included 250 adults, 124 participants MCI, 126 participants. Plasma brain-derived neurotrophic factor (BDNF), irisin clusterin were measured, BDNF/irisin ratio was calculated. Global cognition evaluated by the Montreal Cognitive Assessment. Results: levels, but not BDNF, significantly MCI group group. Higher concentration associated an increased probability both before after controlling covariates. By contrast, BDNF concentration, irisin, linearly correlated performance adjusting ratios only better performance, also lower risks no matter we adjusted concentrations aging, whereas remained stable. No significant results observed. Conclusions: may be a reliable indicator which reflects odds presence directly associates
Language: Английский
Citations
3