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Acod1/itaconate axis controls anxiety-like behaviors induced by chronic infection of Toxoplasma gondii in mice - PubMed
2 months ago
- Chronic infection of Toxoplasma gondii induces anxiety-like behaviors in mice, linked to neuroinflammation.
- The Acod1/itaconate axis plays a key role in regulating these behaviors by modulating neuroinflammation.
- Genetic knockout of Acod1 in mice led to anxiety-like phenotypes, which were reversed by dimethyl itaconate (DI) treatment.
- DI treatment showed both prophylactic and therapeutic benefits, reducing anxiety-like behaviors in infected mice.
- Mechanistically, DI suppresses M1 polarization in microglia via Nrf2 signaling, reducing neuroinflammation and increasing serotonin levels.
- The study suggests the Acod1/itaconate axis as a potential drug target for T. gondii-associated neuropsychiatric conditions.
Prebiotics attenuate depressive-like behavior, neuroinflammation and synaptic plasticity in Parkinson's disease by modulating butyrate-producing gut bacteria - PubMed
2 months ago
- Prebiotics FOS and GOS alleviate depressive-like behavior and motor symptoms in Parkinson's disease (PD).
- Treatment increases brain serotonin and its receptor (SERT), and boosts butyrate-producing gut bacteria.
- Prebiotics reduce intestinal α-synuclein accumulation, inflammation, and improve gut barrier integrity.
- Neuroprotective effects include decreased neuroinflammation markers and preservation of dopaminergic neurons.
- Enhancement of synaptic plasticity via increased expression of BDNF, p-CREB, and synaptic protein PSD-95.
- Study suggests microbiota-gut-brain axis modulation as a therapeutic strategy for PD and depression.
Focusing on microglial mitochondria-lysosome crosstalk and neuroinflammation underlying depression: from molecular pathways to potential therapeutic interventions - PubMed
2 months ago
- Depression is a prevalent emotional disorder with significant global health impacts.
- Neuroinflammation is a key feature of depression, with microglia playing a crucial role in sensing and amplifying inflammation.
- Mitochondria-lysosome contact sites (MLCs) in microglia modulate metabolic states and inflammatory phenotypes.
- Disruption of MLCs leads to ROS accumulation, pro-inflammatory cytokine production, and neuroinflammatory cascades.
- Peripheral immune dysregulation, oxidative stress, and impaired autophagy contribute to neuroinflammation and depressive behaviors.
- Mitochondrial dysfunction and lysosomal pathology amplify inflammatory signaling in depression.
- Microglial MLCs abnormalities involve disrupted Ca²+ crosstalk, impaired autophagic flux, and redox imbalance.
- Emerging therapeutic strategies aim to restore MLC-regulated pathways for neuroinflammation-targeted antidepressant therapies.
SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice - PubMed
2 months ago
- Heart failure (HF) affects over 64 million individuals globally and is linked to cognitive impairment (CI), but the mechanisms are unclear.
- Solute carrier family 22 member 3 (SLC22A3) is identified as a candidate gene for HF-induced CI through Mendelian randomization and bioinformatics analysis.
- A mouse model of HF after myocardial infarction (MI) was used to study SLC22A3's role, with cognitive performance assessed via the Morris water maze.
- HF mice showed downregulated cardiac SLC22A3 expression, increased peripheral histamine (HA) levels, and raised HA levels in the brain.
- Restoring SLC22A3 in HF mice reduced HA accumulation and improved cognitive performance.
- HA breached the compromised blood-brain barrier (BBB) in HF mice, activating hippocampal microglia H1 receptor (H1R) and the NLRP3 inflammasome.
- In BV2 cells, HA stimulation increased NLRP3 expression dose-dependently, blocked by H1R antagonist.
- Knockdown of H1R or NLRP3 in the hippocampus reduced neuroinflammation and rescued HF-induced CI.
- The study reveals a cardio-neuroinflammatory axis driven by SLC22A3 deficiency, with the HA/H1R/NLRP3 pathway as a therapeutic target for HF-induced CI.
Alzheimer's Disease, Circadian Rhythms, and the Immune System: Potential Interconnections - PubMed
2 months ago
- Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by amyloid-β plaques and neurofibrillary tangles.
- Circadian rhythm disruptions (chronodisruption) are linked to AD pathogenesis, affecting metabolism, sleep, and neuroinflammation.
- The immune system, including microglia and astrocytes, plays a central role in AD progression.
- Immune function exhibits circadian variation, and disruptions may impair amyloid-β clearance and promote inflammation.
- Potential therapeutic strategies include melatonin agonists, orexin receptor antagonists, and lifestyle interventions like the Mediterranean diet and physical activity.
- The gut microbiome, influenced by circadian rhythms, may contribute to AD pathophysiology.
- Bidirectional interactions between immune signaling and circadian rhythms highlight a complex regulatory network in AD.
The Protective Effects of Dendrobine on LPS-Induced Neuroinflammation and Related Mechanisms Based on Microglial M1/M2 Polarization - PubMed
2 months ago
- Dendrobine (DDB), an active ingredient in Dendrobium, exhibits neuroprotective properties.
- The study explores DDB's effects on LPS-induced neuroinflammation in BV2 microglial cells.
- DDB significantly reduces NO release and ROS levels in LPS-induced BV2 cells.
- DDB decreases pro-inflammatory mediators (TNF-α, IL-6, IL-1β) and increases anti-inflammatory mediators (IL-10, Arg-1).
- DDB shifts microglial polarization from M1 (pro-inflammatory) to M2 (anti-inflammatory) phenotype.
- Findings suggest DDB as a potential compound for preventing neuroinflammation-related disorders.
Astroglial and Neuronal Injury Markers (GFAP, UCHL-1, NfL, Tau, S100B) as Diagnostic and Prognostic Biomarkers in PTSD and Neurological Disorders - PubMed
2 months ago
- PTSD involves neuroinflammation, glial dysfunction, and neuronal injury.
- Chronic stress leads to BBB disruption, oxidative stress, and neural damage.
- Biomarkers like GFAP, UCHL-1, NfL, Tau, and S100B indicate brain dysfunction in PTSD.
- GFAP and S100B reflect astrocyte activation and BBB permeability.
- UCHL-1, NfL, and Tau indicate neuronal injury and axonal degeneration.
- Altered biomarker levels correlate with symptom severity and cognitive impairment in PTSD.
- These biomarkers may aid in early diagnosis and personalized treatment strategies.
HIV Infection, Neurotoxicity, Inflammation, Premature Aging, and Therapeutic Challenges to PLWH: An Overview - PubMed
2 months ago
- HIV infection remains a major global health challenge due to its complex pathogenesis and lifelong persistence in people living with HIV (PLWH).
- A central barrier to eradication is the virus's ability to establish long-lived latent reservoirs in different tissues, including the central nervous system (CNS).
- In the CNS, HIV persists despite systemic viral suppression because of limited ART penetration across the blood-brain barrier (BBB).
- Modern ART regimens significantly reduce viral burden and HIV-related morbidity but do not eliminate neurocognitive complications.
- Suboptimal CNS drug penetration and certain ART-associated toxicities contribute to CNS dysfunction, persistent neuroinflammation, and accelerated aging of the brain.
- Prolonged exposure to ART and persistent low-level viral activity exacerbate chronic inflammation, immune activation, and metabolic dysregulation, collectively accelerating neurobiological aging.
- These pathological processes contribute to the development of HIV-associated neurocognitive disorders (HAND), which affect nearly half of virally suppressed PLWH.
Deletion of TRPA1 Ion Channel Modulates the Central Stress Responses in a Mouse Model of Posttraumatic Stress Disorder - PubMed
2 months ago
- TRPA1 ion channel deletion affects central stress responses in a PTSD mouse model.
- PTSD involves stress-regulating regions like locus coeruleus (LC) and paraventricular nucleus (PVN).
- Clonidine inhibits LC activity, reducing PTSD symptoms, suggesting noradrenergic involvement.
- TRPA1 is linked to neuroinflammation and stress adaptation.
- Foot shock PTSD model used in Trpa1 wild-type (WT) and knockout (KO) mice.
- Stress increased LC tyrosine hydroxylase (TH) and PVN glial activation.
- Trpa1 KO mice showed exaggerated LC/TH responses but reduced PVN astrocyte activation.
- Clonidine increased freezing and decreased jumping (hyperarousal marker) in WT mice.
- KO mice showed enhanced jumping and no response to clonidine.
- Corticosterone levels remained unchanged in both groups.
- TRPA1 may regulate LC noradrenergic output and PVN neuroinflammation in PTSD.
The role of MyD88 in the nervous system: Neuronal functions, implications in neurological diseases, and therapeutic potential - PubMed
2 months ago
- MyD88 is a key adaptor protein in Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling, playing a role in neuroimmune interactions and neuromodulation.
- MyD88 is expressed widely in the nervous system, influencing both glial cells and neuronal networks, with roles in neurodevelopment and neuroinflammation.
- The article reviews MyD88's involvement in brain injury, chronic pain, and neurodegenerative diseases like Alzheimer's, Parkinson's, and ALS.
- Therapeutic approaches targeting MyD88-dependent pathways are discussed, emphasizing neuroprotective potential and the need for cell-selective therapies.
- The review advocates for more precise and translational MyD88-targeted interventions to improve treatment outcomes.
Targeting TREM2 to disentangle neuroinflammation and α-Syn pathological propagation in Parkinson's disease - PubMed
2 months ago
- Parkinson's disease (PD) is a neurodegenerative disorder affecting the central nervous system, characterized by dopaminergic neuron loss and α-synuclein (α-Syn) aggregation.
- TREM2, a regulator of microglial function, plays a key role in PD by mediating phagocytosis, inflammation, autophagy, and neuronal repair.
- Recent advances highlight the genetic link between TREM2 variants and PD, and TREM2's role in α-Syn propagation and neuroinflammation.
- The review discusses TREM2's molecular structure, signaling mechanisms, and its impact on α-Syn metabolism, microglial polarization, and neuron survival.
- TREM2 gene variants and their interaction with environmental factors are analyzed for their pathological significance in PD.
- Therapeutic strategies targeting TREM2 signaling in PD are reviewed, alongside current research controversies and future directions.
Exploring Neuronal Exosome miRNAs as Biomarkers of Neuroinflammation and Neuroplasticity in Amateur Boxers After Repetitive Head Trauma - PubMed
2 months ago
- Study explores neuron-derived exosomal miRNAs as biomarkers for neuroinflammation and neuroplasticity in amateur boxers after repetitive head trauma.
- Repetitive mild traumatic brain injuries in contact sports like boxing are risk factors for long-term neurodegenerative conditions.
- Neuron-derived exosomes were isolated from plasma samples before and after sparring sessions in ten male athletes.
- Eight miRNAs related to neuroplasticity and inflammation were analyzed, showing significant changes post-sparring.
- Findings suggest neuron-derived exosomal miRNAs could serve as peripheral biomarkers for early detection of sports-related brain injury.
- The study was approved by the Ethics Committee and conducted in accordance with the Declaration of Helsinki.
Cornuside Alleviates Microglia-Mediated Neuroinflammation to Ameliorate Chronic Neuropathic Pain-induced Cognitive Impairment via the Nrf2/Sirt3 Signaling Pathway - PubMed
2 months ago
- Cornuside, derived from Cornus officinalis, shows potential in treating cognitive impairment caused by chronic neuropathic pain (CNP-CI).
- The study highlights cornuside's ability to reduce microglia-mediated neuroinflammation and improve cognitive functions via the Nrf2/Sirt3 pathway.
- Activation of the Nrf2/Sirt3 signaling pathway and enhancement of mitophagy are key mechanisms through which cornuside exerts its effects.
- Inhibition of Sirt3 negates the therapeutic benefits of cornuside, underscoring the pathway's importance in its mechanism of action.
- The findings suggest cornuside as a promising therapeutic candidate for CNP-CI, offering new insights into its pharmacological properties.
Hypoxia-inducible protein 2 mediates metabolic adaptation of Ly6ChighLy6Glow monocytes after stroke - PubMed
2 months ago
- Ly6Chigh monocytes play a critical role in secondary neuroinflammation after stroke.
- Hypoxia-inducible protein 2 (HIG2) mediates metabolic adaptation in Ly6ChighLy6Glow monocytes.
- HIG2 promotes phosphatidylcholine synthesis via Hif1α-dependent regulation of choline kinase α.
- HIG2 initiates lipid metabolism reprogramming, leading to an anti-inflammatory phenotype in monocytes.
- Intranasal delivery of recombinant HIG2 protein improves neurological outcomes post-stroke.
- Targeting HIG2 could be a novel immunometabolic strategy to reduce neuroinflammation after stroke.
Repeatedly occurring retrograde menstruation intensifies central sensitization driven by neuroinflammation in endometriosis models - PubMed
2 months ago
- Chronic pelvic pain (CPP) development was studied using rhesus macaques with naturally occurring endometriosis and a multiple-lesion induction mouse model (MIM).
- Repeated retrograde menstruation is considered an underlying mechanism of endometriosis pathogenesis.
- MIM increased lesion numbers and elevated hypersensitivity, with persistent glial cell activation observed in multiple brain regions and spinal cords.
- Elevated TRPV1, SP, and CGRP expressions in the dorsal root ganglia (DRG) were persistent in MIM.
- MIM induced severe disappearance of TIM4hi MHCIIlo residential macrophages and an influx of pro-inflammatory TIM4lo MHCIIhi macrophages in the peritoneal cavity.
- Cytokine levels were persistently elevated in MIM.
- Dienogest (a synthetic progestin) and fingolimod (a selective immunosuppressor) reduced hyperalgesia and neuroinflammation.
- Recurrent retrograde menstruation can induce nociceptive pain and create a composite chronic inflammatory stimulus, leading to neuroinflammation and central nervous system sensitization.
- Neuroplasticity circuits and peripheral organ stimulation via neuroinflammation feedback loops may mediate widespread endometriosis-associated CPP.
- Findings in mice were supported by results from rhesus macaques with spontaneously developed advanced endometriosis via recurrent retrograde menstruation.
Long-lasting remodeling of astrocytes in an Scna1+/- mouse model of Dravet syndrome - PubMed
2 months ago
- Dravet syndrome (DS) is caused by mutations in the SCN1A gene, leading to loss of function of the Na��1.1 sodium channel.
- The study uses a heterozygous Scn1a knockout (Scn1a+/-) mouse model to explore astrocyte remodeling in DS.
- Increased hippocampal and cortical GFAP transcript and protein levels were observed in Scn1a+/- mice from disease aggravation to long-term stabilization.
- Astrocyte branching increased during the aggravation phase but was not sustained long-term.
- No association was found between astrocyte modifications and macroscopic hippocampal sclerosis or cortical atrophy.
- Long-term astrocyte-astrocyte network expansion and increased connexin protein levels were observed in Scn1a+/- mice.
- Impaired astrocytic hemichannel function was indicated by an ethidium bromide uptake assay.
- Astrocyte remodeling in DS is independent of tissue damage and may be linked to seizures, synaptic, and cognitive deficits.
DRP1 induces neuroinflammation via transcriptional regulation of NF-ĸB - PubMed
2 months ago
- DRP1, known for mitochondrial fission, also acts as a transcription factor regulating neuroinflammation.
- Upon LPS stimulation, DRP1 moves to the nucleus and binds to the Rela promoter, activating NF-κB and inflammatory cytokines.
- The study highlights the role of lipocalin-2 in brain inflammation and identifies DRP1-mediated pathways as potential therapeutic targets for neurodegenerative diseases.
Synergistic disruption of the blood-brain barrier in tree shrews by Methamphetamine and HIV-1 Tat via TRPM2-Mediated astrocyte inflammation - PubMed
2 months ago
- Methamphetamine (METH) and HIV-1 Tat protein (Tat) synergistically disrupt the blood-brain barrier (BBB) in tree shrews.
- The disruption is mediated via TRPM2 channels in astrocytes, leading to neuroinflammation and BBB damage.
- Both in vitro and in vivo models showed that METH and Tat decrease tight junction proteins and increase BBB permeability.
- Pharmacological inhibition or astrocyte-specific knockdown of TRPM2 mitigated BBB damage and neuroinflammation.
- TRPM2 inhibition also alleviated METH + Tat-induced behavioral impairments in tree shrews.
- The study identifies TRPM2 as a potential therapeutic target for neurotoxicity caused by METH and HIV-1 Tat.
Paraquat induces neuroinflammation through glycolysis reprogramming in microglia: evidence from network toxicology analysis and in vitro experiments - PubMed
2 months ago
- Paraquat (PQ) is linked to Parkinson's disease, but the mechanisms are not fully understood.
- Network toxicology analysis predicted PQ targets microglia, causing glucose metabolism disorder.
- PQ enhances glycolysis in BV2 cells, increasing lactate, HK2, GLUT-1 expression, and glycolysis flux.
- PQ activates mTOR and inhibits AMPK, promoting pro-inflammatory polarization in microglia.
- Inhibiting glycolysis or silencing HK2 reduces PQ-induced inflammation and dopaminergic neuron apoptosis.
- Microglial glycolysis reprogramming is a key mechanism in PQ neurotoxicity and neuroinflammation.
- Targeting microglial glycolysis could be a potential intervention for neurodegenerative disorders.
Alterations in GABAergic Interneurons, Neuroinflammation, and Epigenetics: Potential Targets for Therapeutic Strategies in Schizophrenia - PubMed
2 months ago
- Schizophrenia (SZ) is a chronic psychiatric disorder affecting cognition, emotions, and behavior.
- Epigenetic changes during early development disrupt GABAergic-glutamatergic neurotransmission, increasing SZ risk.
- Neuroinflammation, driven by microglial reactivity, contributes to SZ pathology and cognitive impairment.
- GABAergic interneuron markers (somatostatin, parvalbumin) are altered by systemic inflammation.
- TLR4 and NF-κB1 are key molecular targets linked to inflammation and gene regulation in SZ.
- Polyphenols (quercetin, EGCG, resveratrol) and valproic acid show anti-inflammatory and epigenetic therapeutic potential.
- Epigenetic modifications in parvalbumin-positive interneurons and glutamate dysfunction play a role in SZ pathogenesis.

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#neuroinflammation

Acod1/itaconate axis controls anxiety-like behaviors induced by chronic infection of Toxoplasma gondii in mice - PubMed

Prebiotics attenuate depressive-like behavior, neuroinflammation and synaptic plasticity in Parkinson's disease by modulating butyrate-producing gut bacteria - PubMed

Focusing on microglial mitochondria-lysosome crosstalk and neuroinflammation underlying depression: from molecular pathways to potential therapeutic interventions - PubMed

SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice - PubMed

Alzheimer's Disease, Circadian Rhythms, and the Immune System: Potential Interconnections - PubMed

The Protective Effects of Dendrobine on LPS-Induced Neuroinflammation and Related Mechanisms Based on Microglial M1/M2 Polarization - PubMed

Astroglial and Neuronal Injury Markers (GFAP, UCHL-1, NfL, Tau, S100B) as Diagnostic and Prognostic Biomarkers in PTSD and Neurological Disorders - PubMed

HIV Infection, Neurotoxicity, Inflammation, Premature Aging, and Therapeutic Challenges to PLWH: An Overview - PubMed

Deletion of TRPA1 Ion Channel Modulates the Central Stress Responses in a Mouse Model of Posttraumatic Stress Disorder - PubMed

The role of MyD88 in the nervous system: Neuronal functions, implications in neurological diseases, and therapeutic potential - PubMed

Targeting TREM2 to disentangle neuroinflammation and α-Syn pathological propagation in Parkinson's disease - PubMed

Exploring Neuronal Exosome miRNAs as Biomarkers of Neuroinflammation and Neuroplasticity in Amateur Boxers After Repetitive Head Trauma - PubMed

Cornuside Alleviates Microglia-Mediated Neuroinflammation to Ameliorate Chronic Neuropathic Pain-induced Cognitive Impairment via the Nrf2/Sirt3 Signaling Pathway - PubMed

Hypoxia-inducible protein 2 mediates metabolic adaptation of Ly6ChighLy6Glow monocytes after stroke - PubMed

Repeatedly occurring retrograde menstruation intensifies central sensitization driven by neuroinflammation in endometriosis models - PubMed

Long-lasting remodeling of astrocytes in an Scna1+/- mouse model of Dravet syndrome - PubMed

DRP1 induces neuroinflammation via transcriptional regulation of NF-ĸB - PubMed

Synergistic disruption of the blood-brain barrier in tree shrews by Methamphetamine and HIV-1 Tat via TRPM2-Mediated astrocyte inflammation - PubMed

Paraquat induces neuroinflammation through glycolysis reprogramming in microglia: evidence from network toxicology analysis and in vitro experiments - PubMed

Alterations in GABAergic Interneurons, Neuroinflammation, and Epigenetics: Potential Targets for Therapeutic Strategies in Schizophrenia - PubMed