Editorial: Neuroinflammatory aspects in neurological disorders

Frontiers in Molecular Medicine, Journal Year: 2025, Volume and Issue: 5

Published: Feb. 11, 2025

Neuroinflammatory mechanisms provide a common basis for wide range of neurological diseases, which in turn may influence their progression and outcome. A major challenge medical science, Parkinson's disease (PD) is characterized by progressive neuronal loss dysfunction leading to severe cognitive, motor, behavioral impairments. Neuroinflammation the central nervous system (CNS) plays fundamental role PD continues spark off intense debate (Cantero-Fortiz Boada 2024). Alternatively, neuropathic pain arises from injury or somatosensory through immune glial cell invasion. Given neuroinflammation, damage usually outweighs repair process sensitization pathways (Scheuren Calvo On other hand, traumatic brain (TBI), neuroinflammatory show dual component, since it involves activation, inflammatory regulator release, recruitment cells periphery produce secondary injury, at same time also responsible damaged tissue (Zhao et al., 2023). In contrast, Guillain-Barré syndrome (GBS), one most disorders peripheral (PNS), an example how processes mediated T cell, macrophage autoantibodies acute demyelinating (Zarobkiewicz 2021). These diseases highlight neuroinflammation many disbalances.The article Qin al. -https://doi.org/10.3389/fnins.2024.1396345-addresses relevance neurodegenerative such as targeting can become valuable therapeutic tool. To this end, Rhein -an anthraquinone compound bearing anti-inflammatory properties isolated plants aloe vera used Chinese medicine-was assessed agent mouse experimental model PD. This molecule succeeded reducing canonical signaling MAPK/IκB and, consequently, proinflammatory IL-1β, IL-6 TNF-α cytokines substantia nigra striatum. At level, reduced dopaminergic neuron deposition α-synuclein extracellular biomarker injury-and thus attenuated movement disorders.Salniccia -https://doi.org/10.3389/fneur.2023.1289361-have reviewed neural mobilization (NM), physiotherapy technique involving passive limb nerve structures restore structural animal models. The authors found that NM alleviated opioid modulation, with regulatory effects on systems modifications PNS CNS. Beneficial were observed motion, function, postural control, muscle strength endurance. review unveils physiological underlying NM, only be addressed For instance, models have revealed decreases biomarkers NGF, GFAP, substance P, TRPV1 but increases u-opioid receptors, associated higher tolerance pain, dorsal root ganglia. NGF myelin protein zero -related Schwan regeneration, recovery, remyelination-increased, IL-1B decreased nerves. Most importantly, BDNF, OX-42, microglia, key areas periaqueductal grey thalamus following NM. Summing up, studies modulation levels endogenous analgesic systems.A contributor mortality morbidity, TBI defined impairment functionality resulting consciousness, memory, neurological, mental state alterations caused external force. al.- https://doi.org/10.3389/fimmu.2023.1293471-studied relationship between markers white matter integrity rat well clinical cases. Following cortical TBI, rats experienced time-dependent increase immunological IL1b, IL-6, G-CSF, CCL3, CCL5, TNF-α, correlated preservation, fractional anisotropy (FA) index performed diffusion tensor imaging (DTI) MRIs detect axonal injuries. Similar results cases, correlations post-injury period. are contrast evidence showing elevated patients linked negative outcomes. findings obtained paper warn against ambivalent conclusions could drawn use chemokines predict favorable outcomes compared more pathology and/or morbidity.Finally, GBS degenerative neuropathy biases consequence respiratory digestive viral infection. However, case presented here Xu -https://doi.org/10.3389/fimmu.2024.1403561-discusses rare GBS, ischemic brainstem infarction. An elderly woman hospitalized weakness numbness her left limbs walking instability, coincided paramedian pons infarction, bilateral multiple lacunar cerebral infarctions, atherosclerosis, among imaging. patient was initially treated stroke antiplatelet lipid lowering therapy, butyphthalide, edaravone. As symptoms improved, discharged had again due gradual four limbs. Although images showed no bleeding relapse, did not improve, tests potential infectious origin rendered results. argue molecules enter circulation injured blood-brain barrier (BBB) cerebrospinal fluid (CSF), leads immunosuppression auto anti-GD2 antibody ganglioside, autoimmune marker. Accordingly, diagnosed successfully intravenous immunoglobulin.

Language: Английский

NLRP3 inflammasome in neuroinflammation and central nervous system diseases

Cellular and Molecular Immunology, Journal Year: 2025, Volume and Issue: unknown

Published: March 13, 2025

Abstract Neuroinflammation plays an important role in the pathogenesis of various central nervous system (CNS) diseases. The NLRP3 inflammasome is intracellular multiprotein complex composed innate immune receptor NLRP3, adaptor protein ASC, and protease caspase-1. activation can induce pyroptosis release proinflammatory cytokines IL-1β IL-18, thus playing a inflammatory responses. Recent studies have revealed that activated brain to neuroinflammation, leading further neuronal damage functional impairment, contributes pathological process neurological diseases, such as multiple sclerosis, Parkinson’s disease, Alzheimer’s stroke. In this review, we summarize neuroinflammation course CNS diseases discuss potential approaches target for treatment

Language: Английский

Neuroprotective effects of ghrelin in cuprizone-induced rat model of multiple sclerosis

Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(4)

Published: April 11, 2025

Language: Английский