β-Galactosylceramidase Deficiency Causes Upregulation of Long Pentraxin-3 in the Central Nervous System of Krabbe Patients and Mice.

Globoid cell leukodystrophy (GLD), or Krabbe disease, is a neurodegenerative sphingolipidosis caused by genetic deficiency of lysosomal (), characterized by neuroinflammation and demyelination of the central (CNS) and peripheral nervous system. The acute phase protein long pentraxin-3 (PTX3) is a soluble pattern recognition receptor and a regulator of innate immunity. Growing evidence points to the involvement of PTX3 in neurodegeneration.

Vitreous from idiopathic epiretinal membrane patients induces glial-to-mesenchymal transition in Müller cells.

Idiopathic epiretinal membranes (ERMs) are fibrocellular membranes containing extracellular matrix proteins and epiretinal cells of retinal and extraretinal origin. iERMs lead to decreased visual acuity and their pathogenesis has not been completely defined. Macroglial Müller cells appear to play a pivotal role in the pathogenesis of iERM where they may undergo glial-to-mesenchymal transition (GMT), a transdifferentiation process characterized by the downregulation of Müller cell markers, paralleled by the upregulation of pro-fibrotic myofibroblast markers.

VEGF-Independent Activation of Müller Cells by the Vitreous from Proliferative Diabetic Retinopathy Patients.

Proliferative diabetic retinopathy (PDR), a major complication of diabetes mellitus, results from an inflammation-sustained interplay among endothelial cells, neurons, and glia. Even though anti-vascular endothelial growth factor (VEGF) interventions represent the therapeutic option for PDR, they are only partially efficacious. In PDR, Müller cells undergo reactive gliosis, produce inflammatory cytokines/chemokines, and contribute to scar formation and retinal neovascularization.

Gene expression analysis identifies two distinct molecular clusters of idiopatic epiretinal membranes.

Idiopathic epiretinal membranes (ERMs) are fibrocellular membranes containing extracellular matrix proteins and epiretinal cells of retinal and extraretinal origin. iERMs lead to decreased visual acuity and their pathogenesis has not been completely defined. Aim of this study was to provide a molecular characterization of iERMs by gene expression analysis.

Neuroprotective role of naringenin against methylmercury induced cognitive impairment and mitochondrial damage in a mouse model.

Human exposure to organomercurials like methylmercury (MeHg) may occur by consumption of contaminated seafood, affecting various vital organs especially, brain contributing to neuro disorders. The citrus flavanone, naringenin (NAR) has shown strong antioxidant and anti-inflammatory effects and therefore may exert cytoprotective effect against xenobiotic agents. Herein, we investigated the neuroprotective role of NAR against MeHg induced functional changes in mitochondria, neuronal cell death and cognitive impairment in a mouse model.