Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome DOI Creative Commons
Francesca Martina Filannino, Melania Ruggiero, Maria Antonietta Panaro

et al.

Molecules, Journal Year: 2024, Volume and Issue: 29(23), P. 5623 - 5623

Published: Nov. 28, 2024

Neuroinflammation is defined as an immune response involving various cell types, particularly microglia, which monitor the neuroimmune axis. Microglia activate in two distinct ways: M1, pro-inflammatory and capable of inducing phagocytosis releasing factors, M2, has anti-inflammatory properties. Inflammasomes are large protein complexes that form to internal danger signals, activating caspase-1 leading release cytokines such interleukin 1β. Irisin, a peptide primarily released by muscles during exercise, was examined for its effects on BV2 microglial cells vitro. Even at low concentrations, irisin observed influence NLRP3 inflammasome, showing potential neuroprotective agent after stimulation with lipopolysaccharides (LPSs). Irisin helped maintain microglia their typical physiological state reduced migratory capacity. also increased Arg-1 expression, marker M2 polarization, while downregulating NLRP3, Pycard, caspase-1, IL-1β, CD14. The results this study indicate may serve crucial mediator neuroprotection, thus representing innovative tool prevention neurodegenerative diseases.

Language: Английский

Beyond Amyloid and Tau: The Critical Role of Microglia in Alzheimer’s Disease Therapeutics DOI Creative Commons
Daniela Dias, Renato Socodato

Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 279 - 279

Published: Jan. 23, 2025

Alzheimer’s disease (AD) is traditionally viewed through the lens of amyloid cascade hypothesis, implicating amyloid-beta and tau protein aggregates as main pathological culprits. However, burgeoning research points to brain’s resident immune cells, microglia, critical players in AD pathogenesis, progression, potential therapeutic interventions. This review examines dynamic roles microglia within intricate framework AD. We detail involvement these cells neuroinflammation, explaining how their activation response fluctuations may influence trajectory. further elucidate complex relationship between pathology. study highlights dual nature which contribute both aggregation clearance protein. Moreover, an in-depth analysis interplay unveils significant, yet often overlooked, impact this interaction on neurodegeneration Shifting from conventional approaches, we assess current treatments primarily targeting introduce novel strategies that involve manipulating microglial functions. These innovative methods herald a paradigm shift management Finally, explore field precision diagnosis pursuit robust biomarkers. underline more profound comprehension biology could enrich essential areas, potentially paving way for accurate diagnostic tools tailored treatment strategies. In conclusion, expands perspective pathology treatment, drawing attention multifaceted microglia. As continue enhance our understanding microglial-focused interventions emerge promising frontier bolster arsenal fight against

Language: Английский

Citations

1
Combination of tauroursodeoxycholic acid, co-enzyme Q10 and creatine demonstrates additive neuroprotective effects in in-vitro models of Parkinson’s disease DOI Creative Commons
Alexander Shtilbans, Wolfgang Reintsch, Valerio E. C. Piscopo

et al.

Frontiers in Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Dec. 23, 2024

This study aimed to evaluate different combinations of three dietary supplements for potential additive or synergistic effects in an vitro Parkinson’s Disease model. The complex and diverse processes leading neurodegeneration each patient with a neurodegenerative disorder cannot be effectively addressed by single medication. Instead, various potentially neuroprotective agents targeting disease mechanisms simultaneously may show improved efficacy slowing the progression allowing utilized at lower doses minimize side effects. We evaluated four possible selected supplements: tauroursodeoxycholic acid (TUDCA), co-enzyme Q10 (CoQ10), creatine, chosen their on targets that had previously shown preclinical models. following combinations: (1) TUDCA+CoQ10, (2) TUDCA+Creatine, (3) CoQ10 + Creatine, (4) TUDCA+CoQ10 Creatine. used induced pluripotent stem cell (iPSC) derived human dopaminergic neurons from healthy control, as well microglial cells, effect these neuroinflammation. neurofilament heavy chain, tubulin filament, proinflammatory cytokines metrics. have identified triple combination showed protective across all endpoints. Indeed, could address majority known pathways neurodegeneration, such accumulation misfolded α -synuclein, mitochondrial dysfunction, reactive oxygen species, demonstrated TUDCA, CoQ10, creatine exerts models disease, surpassing compound individually. shows strong candidate further confirmatory studies clinical trials treatment patients with, risk for, disease.

Language: Английский

Citations

2
Advances in induced pluripotent stem cell-based in vitro disease modeling for rare neurodegenerative disease: A narrative review DOI Creative Commons

Seung‐Yeon Lee,

Hyo Jin Son, Sang Won Seo

et al.

Precision and Future Medicine, Journal Year: 2024, Volume and Issue: 8(3), P. 65 - 73

Published: Sept. 6, 2024

Understanding the genetic basis and pathomechanisms underlying dementia arising from single-gene mutations is crucial to expand our knowledge in field of research. In this review, we comprehensively summarize results existing research using induced pluripotent stem cells (iPSCs) investigate familial Alzheimer’s disease caused by presenilin-1 (PSEN1), presenilin-2 (PSEN2), or amyloid precursor protein (APP) genes. We further review iPSC studies leukodystrophies, including Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts Leukoencephalopathy (CADASIL), notch receptor 3 (NOTCH3) gene; adult-onset leukoencephalopathy axonal spheroids pigmented glia (ALSP), colony-stimulating factor 1 (CSF1R) gene. systematically advantages necessity iPSCs elucidate pathogenesis neurodegenerative diseases, particularly facilitate modeling. Furthermore, introduce applied based on technology. Through aimed help mechanisms which causative genes induce symptoms would contribute development effective treatment strategies.

Language: Английский

Citations

0
Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome DOI Creative Commons
Francesca Martina Filannino, Melania Ruggiero, Maria Antonietta Panaro

et al.

Molecules, Journal Year: 2024, Volume and Issue: 29(23), P. 5623 - 5623

Published: Nov. 28, 2024

Neuroinflammation is defined as an immune response involving various cell types, particularly microglia, which monitor the neuroimmune axis. Microglia activate in two distinct ways: M1, pro-inflammatory and capable of inducing phagocytosis releasing factors, M2, has anti-inflammatory properties. Inflammasomes are large protein complexes that form to internal danger signals, activating caspase-1 leading release cytokines such interleukin 1β. Irisin, a peptide primarily released by muscles during exercise, was examined for its effects on BV2 microglial cells vitro. Even at low concentrations, irisin observed influence NLRP3 inflammasome, showing potential neuroprotective agent after stimulation with lipopolysaccharides (LPSs). Irisin helped maintain microglia their typical physiological state reduced migratory capacity. also increased Arg-1 expression, marker M2 polarization, while downregulating NLRP3, Pycard, caspase-1, IL-1β, CD14. The results this study indicate may serve crucial mediator neuroprotection, thus representing innovative tool prevention neurodegenerative diseases.

Language: Английский

Citations

0