Microglia regulate motor neuron plasticity via reciprocal fractalkine and adenosine signaling DOI Creative Commons
Alexandria B. Marciante,

Arash Tadjalli,

Mária Nikodémová

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: Nov. 28, 2024

Language: Английский

Calcium (Ca2+) signaling in plants: A plant stress perspective DOI
Misbah Naz, Muhammad Afzal,

Muhammad Ammar Raza

et al.

South African Journal of Botany, Journal Year: 2024, Volume and Issue: 169, P. 464 - 485

Published: May 4, 2024

Language: Английский

Citations

9

Surface-Enhanced Raman Scattering Nanosensing and Imaging in Neuroscience DOI

Ryma Boudries,

Hannah Williams,

Soraya Paquereau--Gaboreau

et al.

ACS 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

9

Oral ATP treatment in alternating hemiplegia of childhood: a case report and review DOI Creative Commons
Marco Carrozzi, Maria Elisa Morelli, Mario Cirino

et al.

Frontiers 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

1

Blockade of A2AR improved brain perfusion and cognitive function in a mouse model of Alzheimer’s disease DOI
Mariana Sayuri Berto Udo, Julia Zaccarelli‐Magalhães, Garrett A. Clemons

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 22, 2025

Language: Английский

Citations

0

Platelets tune fear memory in mice DOI Creative Commons
Stefano Garofalo, Alessandro Mormino,

L. Mazzarella

et al.

Cell 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

0

Purinergic System Transcript Changes in the Dorsolateral Prefrontal Cortex in Suicide and Major Depressive Disorder DOI Open Access
Smita Sahay, Anna Lundh,

Roshan P. Sirole

et al.

International 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

0

Purine Metabolism and Dystonia: Perspectives of a Long‐Promised Relationship DOI Creative Commons
Ugo Sorrentino, Audrey G. O’Neill, Justin M. Kollman

et al.

Annals 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

0

Mechanisms of astrocytic and microglial purinergic signaling in homeostatic regulation and implications for neurological disease DOI Creative Commons
Moawiah M. Naffaa

Exploration 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

0

Expanding the Allelic and Clinical Heterogeneity of Movement Disorders Linked to Defects of Mitochondrial Adenosine Triphosphate Synthase DOI Creative Commons

Philip Harrer,

Magdalena Krygier, Martin Krenn

et al.

Movement 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

0

Dual role for pannexin 1 at synapses: regulating functional and morphological plasticity DOI Creative Commons

Adriana Casillas Martinez,

Leigh E. Wicki‐Stordeur, Annika V. Ariano

et al.

The 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

1