Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 62(4), P. 4576 - 4590
Published: Oct. 28, 2024
Language: Английский
Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 62(4), P. 4576 - 4590
Published: Oct. 28, 2024
Language: Английский
CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(5)
Published: May 1, 2024
Abstract Aims The molecular mechanism of short‐sleep conditions on cognition remains largely unknown. This research aimed to investigate associations between short sleep, inflammatory biomarkers and cognitive function in the US population (NHANES data 2011–2014) explore cellular mechanisms mice. Methods Systemic immune‐inflammation index (SII) was calculated using blood‐cell based biomarkers. Further, we employed integrated bioinformatics single‐cell transcriptomics (GSE137665) examine how sleep exposure influenced pathways associated with inflammation brain. To signaling biological processes deprivation, carried out enrichment analyses utilizing GO KEGG databases. Results Population results showed that, compared normal group, severe lower ability all four tests. Moreover, a higher SII level correlated scores In mice study, elevated activation pathway observed cell subgroups neurons within deprivation recovery cohorts. Additionally, heightened expression oxidative stress response noted GABAergic during deprivation. Conclusion study contributed understanding influence its mechanisms.
Language: Английский
Citations
35Cells, Journal Year: 2025, Volume and Issue: 14(1), P. 54 - 54
Published: Jan. 5, 2025
Neuroinflammation is a complex and multifaceted process that involves dynamic interactions among various cellular molecular components. This sophisticated interplay supports both environmental adaptability system resilience in the central nervous (CNS) but may be disrupted during neuroinflammation. In this article, we first characterize key players neuroimmune interactions, including microglia, astrocytes, neurons, immune cells, essential signaling molecules such as cytokines, neurotransmitters, extracellular matrix (ECM) components, neurotrophic factors. Under homeostatic conditions, these elements promote cooperation stability, whereas neuroinflammatory states, they drive adaptive responses become pathological if dysregulated. We examine how mediated through actors pathways, create networks regulate CNS functionality respond to injury or inflammation. To further elucidate dynamics, provide insights using multilayer network (MLN) approach, highlighting interconnected nature of under inflammatory conditions. perspective aims enhance our understanding communication mechanisms underlying shifts from homeostasis Applying an MLN approach offers more integrative view adaptability, helping clarify processes identify novel intervention points within layered landscape responses.
Language: Английский
Citations
3Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 161, P. 114474 - 114474
Published: March 4, 2023
Alzheimer's disease (AD) is a neurodegenerative mainly characterized by progressive cognitive dysfunction and memory impairment. Recent studies have shown that regulating silent information regulator 1 (SIRT1) expression has significant neuroprotective effect, SIRT1 may become new therapeutic target for AD. Natural molecules are an important source of drug development use in AD therapy regulate wide range biological events as well other SIRT1-mediated signaling pathways. This review aims to summarize the correlation between identify vivo vitro investigating anti-AD properties natural modulators A literature search was conducted published January 2000 October 2022 using various databases, including Web Science, PubMed, Google Scholar, Science Direct, EMBASE. molecules, such resveratrol, quercetin, icariin, bisdemethoxycurcumin, dihydromyricetin, salidroside, patchouli, sesamin, rhein, ligustilide, tetramethoxyflavanone, 1-theanine, schisandrin, curcumin, betaine, pterostilbene, ampelopsin, schisanhenol, eriodictyol, potential modulate pathways, thereby combating The modulating discussed this provide potentially novel multi-mechanistic strategy However, future clinical trials need be further investigate their beneficial determine safety efficacy activators against
Language: Английский
Citations
25Life Sciences, Journal Year: 2024, Volume and Issue: 345, P. 122610 - 122610
Published: April 4, 2024
Language: Английский
Citations
9Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: May 16, 2024
Importance Research is beginning to elucidate the sophisticated mechanisms underlying microbiota-gut-brain-immune interface, moving from primarily animal models human studies. Findings support dynamic relationships between gut microbiota as an ecosystem (microbiome) within (host) and its intersection with host immune nervous systems. Adding this effects on epigenetic regulation of gene expression further complicates strengthens response. At heart inflammation, which manifests in a variety pathologies including neurodegenerative diseases such Alzheimer’s disease, Parkinson’s Multiple Sclerosis (MS). Observations Generally, research date limited has focused bacteria, likely due simplicity cost-effectiveness 16s rRNA sequencing, despite lower resolution inability determine functional ability/alterations. However, omits all other fungi, viruses, phages, are emerging key members microbiome. Much been done pre-clinical and/or small studies more developed parts world. The observed promising but cannot be considered reliable or generalizable at time. Specifically, causal determined currently. More followed by then little MS. data for MS encouraging this. Conclusions relevance While still nascent, interface may missing link, hampered our progress understanding, let alone preventing, managing, putting into remission diseases. Relationships must first established humans, have shown poorly translate complex physiology environments, especially when investigating microbiome where often overly simplistic. Only can robust conducted humans using mechanistic model
Language: Английский
Citations
9Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(7), P. 831 - 831
Published: June 25, 2024
Histamine performs dual roles as an immune regulator and a neurotransmitter in the mammalian brain. The histaminergic system plays vital role regulation of wakefulness, cognition, neuroinflammation, neurogenesis that are substantially disrupted various neurodegenerative neurodevelopmental disorders. H3 receptor (H3R) antagonists inverse agonists potentiate endogenous release brain histamine have been shown to enhance cognitive abilities animal models several Microglial activation subsequent neuroinflammation implicated impacting embryonic adult neurogenesis, contributing development Alzheimer's disease (AD), Parkinson's (PD), autism spectrum disorder (ASD). Acknowledging importance microglia both neurodevelopment, well their by histamine, offers intriguing therapeutic target for these inhibition H3Rs has found facilitate shift from proinflammatory M1 state anti-inflammatory M2 state, leading reduction activity microglial cells. Also, pharmacological studies demonstrated H3R showed positive effects reducing biomarkers, suggesting potential simultaneously modulating crucial neurotransmissions signaling cascades such PI3K/AKT/GSK-3β pathway. In this review, we highlight addressing pathology decline disorders, e.g., AD, PD, ASD, with inflammatory component.
Language: Английский
Citations
9Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(1)
Published: Jan. 7, 2025
Language: Английский
Citations
1Journal of Molecular Neuroscience, Journal Year: 2025, Volume and Issue: 75(1)
Published: Jan. 15, 2025
Language: Английский
Citations
1Journal of Alzheimer s Disease, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 2, 2025
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-β plaques, neurofibrillary tangles, and chronic neuroinflammation. Microglial cells, resident immune cells in central nervous system, play crucial role pathogenesis AD. Microglia can undergo polarization, shifting between pro-inflammatory (M1) anti-inflammatory (M2) phenotypes response to different stimuli. Dysregulation microglial polarization towards phenotype leads release inflammatory cytokines, oxidative stress, synaptic dysfunction. These processes contribute neuronal damage cognitive decline However, several challenges remain this field. The complex molecular mechanisms governing AD need be further elucidated. In review, we discuss underlying its implications progression.
Language: Английский
Citations
1Neurochemistry International, Journal Year: 2025, Volume and Issue: unknown, P. 105946 - 105946
Published: Feb. 1, 2025
Language: Английский
Citations
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