
Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)
Published: Nov. 28, 2024
Language: Английский
Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)
Published: Nov. 28, 2024
Language: Английский
South African Journal of Botany, Journal Year: 2024, Volume and Issue: 169, P. 464 - 485
Published: May 4, 2024
Language: Английский
Citations
9ACS Nano, Journal Year: 2024, Volume and Issue: 18(34), P. 22620 - 22647
Published: Aug. 1, 2024
Monitoring neurochemicals and imaging the molecular content of brain tissues
Language: Английский
Citations
9Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11
Published: Jan. 7, 2025
Alternating hemiplegia of childhood (AHC) is a rare neurological disorder that usually manifests before 18 months age and characterized by recurrent, alternating episodes hemiparesis with variable frequency can last from few minutes to several days. We present case AHC in little girl carrying sporadic mutation the ATP1A3 gene (p.Glu815Lys) refractory flunarizine non-compliant topiramate due adverse effects treated oral compound adenosine-5'-triphosphate (ATP) capsules. Outcome was evaluated through follow-up side safety were monitored regularly. Compounded drug showed effectiveness safety. Indeed, during four-year follow-up, dose gradually increasing up 21 mg/kg, patient substantial benefit controlling duration hemiplegic an improvement deterioration.
Language: Английский
Citations
1GeroScience, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 22, 2025
Language: Английский
Citations
0Cell Reports, Journal Year: 2025, Volume and Issue: 44(2), P. 115261 - 115261
Published: Feb. 1, 2025
Highlights•Platelets are key link in body-brain communication homeostasis•Platelets tune parvalbumin neuron activity and long-term potentiation the hippocampus•Natural killer cells release IL-13 gut with effects on serotonin uptake by platelets•Platelets NK fear memory miceSummarySeveral lines of evidence have shown that platelet-derived factors molecules brain-body pathological conditions. Here, we identify platelets as actors modulation behaviors mice through control inhibitory neurotransmission plasticity hippocampus. Interfering platelet number or activation reduces hippocampal (5-HT) modulates learning mice, this effect is reversed replacement precursor (5-HTP)/benserazide. In addition, unravel natural (NK) participate mechanism, regulating interleukin-13 (IL-13) levels gut, production enterochromaffin platelets. Both depletion reduce neurons increase synaptic transmission. Understanding role neuro-immune interactions offers additional tools for definition molecular cellular elements involved growing field communication.Graphical abstract
Language: Английский
Citations
0International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 1826 - 1826
Published: Feb. 20, 2025
Suicide is a major public health priority, and its molecular mechanisms appear to be related imbalanced purine metabolism in the brain. This exploratory study investigates purinergic gene expression postmortem dorsolateral prefrontal cortex (DLPFC) tissue isolated from subjects with depressive disorder (MDD) who died by suicide (MDD-S, n = 10), MDD did not die (MDD-NS, 6) non-psychiatrically ill controls (CTL, 9–10). Purinergic system transcripts were assayed quantitative polymerase chain reactions (qPCR) superficial deep gray matter as well white DLPFC cortical layers using laser microdissection (LMD). Across all subjects, regardless of sex, P2RY12 (F(2,23) 5.40, p 0.004) P2RY13 (KW statistic 11.82, 0.001) transcript levels significantly greater MDD-S compared MDD-NS subjects. Several other perturbations observed females: NT5E (F(2,10) 13.37, (F(2,9) 3.99, 0.011, controlled for age) was vs. female groups. ENTPD2 5.20, 0.03), ENTPD3 28.99, < 0.0001), among whose elevated CTL Transcripts that exhibited altered included ENTPD2, NT5E, PANX1, (p ≤ 0.05). Our medication analysis revealed these antidepressants. first holistically quantify metabolic pathway utilizing human brain tissue. preliminary findings support evidence implicating changes P2 receptors provide broader dysregulation mood disorders.
Language: Английский
Citations
0Annals of Neurology, Journal Year: 2025, Volume and Issue: unknown
Published: March 3, 2025
Dystonia research focuses on the identification of converging biological pathways, allowing to define molecular drivers that serve as treatment targets. We summarize evidence supporting concept aberrations in purine metabolism intersect with dystonia pathogenesis. The recent discovery IMPDH2 ‐related introduced a gain‐of‐function paradigm purinergic system defects, offering new perspectives understand purine‐pool imbalances brain diseases. discuss commonalities between known dystonia‐linked mechanisms and emerging from studies disorders including Lesch–Nyhan disease. Together, we hypothesize greater appreciation relevance perturbances can offer fresh avenues for therapeutic intervention. ANN NEUROL 2025
Language: Английский
Citations
0Exploration of neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: March 11, 2025
Purinergic signaling, mediated by ATP and adenosine receptors, plays a crucial role in cellular communication homeostasis within the central nervous system (CNS), particularly regulating synaptic activity, glial cell functions, neuroplasticity. Glial cells, including astrocytes microglia, contribute to both short-term processes, such as neurotransmission neuroinflammation, long-term remodeling, tissue repair, behavioral adaptation. Dysregulation of purinergic signaling these cells has been implicated pathogenesis various neurodegenerative neuropsychiatric disorders. This article explores evolving concept synapse, highlighting active modulation emphasizing significance function responses conditions injury neurotoxicity. Specifically, it examines roles receptors—such P2X4, P2X7, P2Y1, P2Y12—in mediating key astrocytic microglial phagocytosis, plasticity, neuronal damage. Furthermore, discusses involvement receptors neurological disorders epilepsy, Alzheimer’s disease, Parkinson’s multiple sclerosis, ischemic stroke, Rett syndrome, autism spectrum disorder, well potential therapeutic strategies targeting mitigate inflammation, promote improve clinical outcomes.
Language: Английский
Citations
0Movement Disorders, Journal Year: 2025, Volume and Issue: unknown
Published: April 25, 2025
Abstract Background Defects of mitochondrial ATP synthase (ATPase) represent an emerging, yet incompletely understood group neurodevelopmental diseases with abnormal movements. Objective The aim this study was to redefine the phenotypic and mutational spectrum movement disorders linked ATPase subunit‐encoding genes ATP5F1A ATP5F1B . Methods We recruited regionally distant patients who had been genome or exome sequenced. Fibroblast cultures from two were established perform RNA sequencing, immunoblotting, mass spectrometry–based high‐throughput quantitative proteomics, activity assays. In silico three‐dimensional missense variant modeling performed. Results identified a patient developmental delay, myoclonic dystonia, spasticity carried heterozygous frameshift c.1404del (p.Glu469Serfs*3) in patient's cells exhibited significant reductions mRNA, underexpression α‐subunit association other aberrantly expressed components, compromised activity. addition, novel deleterious c.1252G>A (p.Gly418Arg) discovered, shared by three families hereditary spastic paraplegia (HSP). This mapped functionally important intersubunit communication site. A third variant, c.1074+1G>T, affected canonical donor splice site resulted exon skipping significantly diminished mRNA levels, as well impaired associated phenotype consisted cerebral palsy (CP) prominent generalized dystonia. Conclusions Our data confirm expand role dominant variants disorders. / ‐related should be considered cause HSP, CP. © 2025 Author(s). Movement Disorders published Wiley Periodicals LLC on behalf International Parkinson Disorder Society.
Language: Английский
Citations
0The Journal of Physiology, Journal Year: 2024, Volume and Issue: unknown
Published: Sept. 12, 2024
Abstract Pannexin 1 (PANX1) is an ion and metabolite membrane channel scaffold protein enriched in synaptic compartments of neurons the central nervous system. In addition to a well‐established link between PANX1 plasticity, we recently identified role for regulation dendritic spine stability. Notably, its interacting proteins are linked neurological conditions involving loss. Understanding dual function morphology may help shed light on these links. We explore potential mechanisms, including PANX1's interactions with postsynaptic receptors cytoskeleton regulating proteins. Finally, contextualize within diseases synapse dysfunction. image
Language: Английский
Citations
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