Biomedical Signal Processing and Control, Journal Year: 2024, Volume and Issue: 96, P. 106601 - 106601
Published: June 28, 2024
Language: Английский
Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)
Published: Feb. 7, 2025
Mitochondrial dysfunction is a pivotal instigator of neuroinflammation, with mitochondrial DNA (mtDNA) leakage as critical intermediary. This review delineates the intricate pathways leading to mtDNA release, which include membrane permeabilization, vesicular trafficking, disruption homeostatic regulation, and abnormalities in dynamics. The escaped activates cytosolic sensors, especially cyclic gmp-amp synthase (cGAS) signalling inflammasome, initiating neuroinflammatory cascades via pathways, exacerbating spectrum neurological pathologies. therapeutic promise targeting discussed detail, underscoring necessity for multifaceted strategy that encompasses preservation homeostasis, prevention leakage, reestablishment dynamics, inhibition activation sensors. Advancing our understanding complex interplay between neuroinflammation imperative developing precision interventions disorders.
Language: Английский
Citations
3
CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(8)
Published: Aug. 1, 2024
Abstract Synaptic plasticity is believed to underlie the cellular and molecular basis of memory formation. Mitochondria are one main organelles involved in metabolism energy maintenance as plastic that change morphologically functionally response needs regulate synaptic function through multiple mechanisms, including ATP generation, calcium homeostasis, biogenesis. An increased neuronal activity enhances efficiency, during which mitochondria's spatial distribution morphology significantly. These build up pre‐and postsynaptic zones produce ATP, necessary for several processes like neurotransmitter release recycling. also homeostasis by buffering intracellular calcium, ensures proper activity. Furthermore, mitochondria presynaptic terminal have distinct morphological properties compared dendritic or mitochondria. This specialization enables precise control plasticity. Mitochondrial dysfunction has been linked failure many neurodegenerative disorders, Alzheimer's disease (AD). In AD, malfunctioning cause delays vesicle recycling, ionic gradient imbalances, mostly failure. review emphasizes mitochondrial plasticity's contribution function. It explores profound effect malfunction on focusing provides an overview how they sustain health under normal conditions their contributes diseases, highlighting potential a therapeutic target such conditions.
Language: Английский
Citations
13
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 5, 2025
Language: Английский
Citations
1
Frontiers in Neuroscience, Journal Year: 2024, Volume and Issue: 18
Published: Feb. 20, 2024
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that affects over 50 million elderly individuals worldwide. Although the pathogenesis of AD not fully understood, based on current research, researchers are able to identify potential biomarker genes and proteins may serve as effective targets against AD. This article aims present comprehensive overview recent advances in identification, with highlights use various algorithms, exploration relevant biological processes, investigation shared biomarkers co-occurring diseases. Additionally, this includes statistical analysis key reported research literature, identifies intersection AD-related gene sets from databases such AlzGen, GeneCard, DisGeNet. For these sets, besides enrichment analysis, protein–protein interaction (PPI) networks utilized central among overlapping genes. Enrichment protein network tissue-specific connectedness GTEx database performed multiple groups Our work has laid foundation for better understanding molecular mechanisms more accurate identification markers.
Language: Английский
Citations
6
Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)
Published: Oct. 3, 2024
Mitochondrial dysfunction (MD) is increasingly recognized as a key pathophysiological contributor in Alzheimer disease (AD). As differential MD genes expression may serve either causative factor or consequence AD, and of these could be influenced by epigenetic modifications interact with inflammatory cytokines, hence, the precise role AD remains uncertain.
Language: Английский
Citations
6
Aging and Health Research, Journal Year: 2023, Volume and Issue: 3(4), P. 100169 - 100169
Published: Nov. 8, 2023
Alzheimer's disease (AD) is a neurodegenerative with reduced cognitive function due to mitochondrial dysfunction and oxidative stress. Recent studies show that the pathophysiology of AD may be influenced by dysfunctionality, Ca2+ imbalance, apoptosis, decreased energy, alteration in its metabolism. Study indicates damaged mitochondria play critical roles pathogenesis AD, even if precise mechanism behind remains unknown. It thought healthy pool protects neurons reducing damage caused also promotes neuronal activity giving enough energy other associated functions. In this sense, investigation mechanisms altered constitutes novel, promising therapeutic targets for disease. Mitochondria enhances generation, antioxidants scavenge reactive oxygen species reduce substrate supply, glucose metabolism, potential drug candidates target apoptotic mitophagy pathways remove mitochondria. Although therapy approaches have shown promise preclinical studies, there hasn't been much advancement clinical trials thus far. Therefore, we try find out role highlight development compounds as AD.
Language: Английский
Citations
12
Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 93, P. 102172 - 102172
Published: Dec. 15, 2023
Language: Английский
Citations
11
Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 362 - 362
Published: Feb. 5, 2025
Background: Recent research indicates that lipid metabolism and autophagy play crucial roles in the development of Alzheimer’s disease (AD). Investigating relationship between AD diagnosis gene expression related to metabolism, autophagy, lipophagy may improve early identification therapeutic targets. Methods: Transcription datasets from patients were obtained Gene Expression Omnibus (GEO). Genes associated with sourced Set Enrichment Analysis (GSEA) database Human Autophagy Database (HADb). Lipophagy-related hub genes identified using a combination Limma analysis, weighted co-expression network analysis (WGCNA), machine learning techniques. Based on these genes, we developed an risk prediction nomogram validated its diagnostic accuracy three external validation datasets. Additionally, levels assessed through quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: Our genes—ACBD5, GABARAPL1, HSPA8—as being progression. The constructed achieved area under curve (AUC) value 0.894 for prediction, all sets yielding AUC values greater than 0.8, indicating excellent efficacy. qRT-PCR results further corroborated associations development. Conclusions: This study lipophagy-related reliable model, offering insights into pathology facilitating patients.
Language: Английский
Citations
0
Journal of Applied Toxicology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 20, 2025
The increasing prevalence of environmental pollutants has raised public concern about their potential role in diseases such as atherosclerosis (AS). Existing studies suggest that chemicals, including bisphenol S (BPS), may adversely affect cardiovascular health, but the specific mechanisms remain unclear. This study aims to elucidate effects BPS on AS and underlying mechanisms. Through an extensive search databases ChEMBL, STITCH, SwissTargetPrediction, SuperPred, SEA, GEO, we identified 34 targets related BPS-induced AS. A target network was constructed using STRING platform Cytoscape software. GO KEGG functional enrichment analysis DAVID database revealed promote occurrence by interfering with critical biological processes glutathione metabolism, nitrogen tyrosine metabolism. followed selection 4 core targets-aminopeptidase n (ANPEP), alcohol dehydrogenase 5 (ADH5), lysosomal pro-x carboxypeptidase (PRCP), microsomal s-transferase 1 (MGST1)-using five machine learning methods. These play a pivotal Furthermore, molecular docking confirmed tight binding between these targets. In conclusion, this provides theoretical framework for understanding contributes scientific evidence development prevention treatment strategies triggered exposure.
Language: Английский
Citations
0
Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)
Published: March 10, 2025
Abstract Spinal cord injury (SCI) can cause permanent dysfunction proceeding from multifaceted neuroinflammatory processes that contribute to damage and repair. Fidgetin-like 2 (FL2), a microtubule-severing enzyme negatively regulates axon growth, microglial functions, wound healing, has emerged as potential therapeutic target for central nervous system injuries neuroinflammation. To test the hypothesis FL2 knockdown increases acute neuroinflammation improves recovery after SCI, we examined effects of nanoparticle-encapsulated siRNA treatment moderate contusion SCI in rats. significantly increased expression lesion site rostral 1 day post-injury (dpi). A single led modestly improved locomotor consistent with preservation corticospinal tract function, accompanied by reduced inflammation presence oligodendrocytes. In determining treatment, RNA sequencing gene set enrichment analyses revealed modulates early cellular responses, including chemokine signaling, both pro- anti-inflammatory immune reactions, neurotransmitter signaling pathways at 1, 4, 7 dpi. Follow-up 4 dpi using dual situ hybridization immunohistochemistry demonstrated mRNA was colocalized microglia/macrophages. downregulation resulted marked accumulation microglia site, inflammatory markers (IL-1β, TGF-β1, CD68). The results suggest induces an increase undermines responses well spinal integrity growth. Overall, our study suggests targeting holds promise strategy treating SCI.
Language: Английский
Citations
0