The objective of the present work was to evaluate on the basis of the authors' data and data in the literature the role of phospholipase A2 in the pathogenesis of schizophrenia. The authors submit available literature pertaining to the problem as well as their own experimental findings. Based on the submitted facts, it cannot be states that phospholipase A2 is a specific marker of schizophrenia.
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Int J Mol Sci
December 2024
Department of Psychiatry, Tufts University School of Medicine, Boston, MA 02111, USA.
Cognitive impairment is a core feature of neurodevelopmental (schizophrenia) and aging-associated (mild cognitive impairment and Alzheimer's dementia) neurodegenerative diseases. Limited efficacy of current pharmacological treatments warrants further search for new targets for nootropic interventions. The breakdown of myelin, a phospholipids axonal sheath that protects the conduction of nerve impulse between neurons, was proposed as a neuropathological abnormality that precedes and promotes the deposition of amyloid-β in neuritic plaques.
View Article and Find Full Text PDFSchizophrenia (Heidelb)
November 2024
Computational Biology and Animal Imaging Centre (CBAC), Tianjin Anding Hospital, Tianjin Medical University Affiliated Tianjin Anding Hospital, Tianjin, 300222, China.
Neural Regen Res
March 2025
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Tropomyosin receptor kinase B (TrkB) signaling plays a pivotal role in dendritic growth and dendritic spine formation to promote learning and memory. The activity-dependent release of brain-derived neurotrophic factor at synapses binds to pre- or postsynaptic TrkB resulting in the strengthening of synapses, reflected by long-term potentiation. Postsynaptically, the association of postsynaptic density protein-95 with TrkB enhances phospholipase Cγ-Ca2+/calmodulin-dependent protein kinase II and phosphatidylinositol 3-kinase-mechanistic target of rapamycin signaling required for long-term potentiation.
View Article and Find Full Text PDFSchizophrenia (Heidelb)
May 2024
Department of Epidemiology and Biostatistics, School of Public Health, Jilin University, Changchun, Jilin, China.
Phospholipase A2(PLA2) superfamily is recognized as being involved in the pathogenesis of schizophrenia by affecting lipid homeostasis in cell membranes. We hypothesized that PLA2 gene copy number variation (CNV) may affect PLA2 enzyme expression and be associated with schizophrenia risk. This study indicated that in the discovery stage, an increased copy number of PLA2G6 and the deletion of PLA2G3, PLA2G4A, PLA2G4F and PLA2G12F was associated with increased risk of schizophrenia.
View Article and Find Full Text PDFInt J Tryptophan Res
March 2024
Department of Psychiatry, Tufts University School of Medicine, Boston MA, USA.
Introduction: Limited clinical efficiency of current medications warrants search for new antipsychotic agents. Deorphanized G-protein coupled receptor (GPR)109A has not attracted much of attention of schizophrenia researchers. We analyzed literature and our data on endogenous agonists of GPR109A, beta-hydroxybutyrate (BHB), anthranilic (AA), butyric (BA), and nicotinic (NA) acids, in individuals with schizophrenia.
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