Editorial: Glial Cells, Maladaptive Plasticity, and Neurodegeneration: Mechanisms, Targeted Therapies, and Future Directions

• Published in: Frontiers in cellular neuroscience Vol. 15; p. 682524
• Main Authors: Korai, Sohaib Ali, Sepe, Giovanna, Luongo, Livio, Cragnolini, Andrea Beatriz, Cirillo, Giovanni
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 30.04.2021; Frontiers Media S.A
• Subjects: Adenosine; Apoptosis; Astrocytes; Bax protein; Bcl-2 protein; Blood-brain barrier; Brain research; Caspase-3; Cellular Neuroscience; Disease; Editorials; Extracellular matrix; Glial cells; Glial plasticity; Homeostasis; Inflammasomes; Inflammation; Interleukin 1; Metabolism; Microglia; MPP; Neural networks; Neurodegeneration; neuroinflammation; Neuronal-glial interactions; Neuroprotection; Oligodendrocytes; p53 Protein; Pathogenesis; Proteins; Regeneration; Signal transduction; synaptic homeostasis; Synaptic plasticity; Synaptic transmission; neurodegeneration; glial cells; synaptic plasticity; synaptic homeostasis; neuroinflammation
• ISSN: 1662-5102; 1662-5102
• DOI: 10.3389/fncel.2021.682524

Glial cells, including astrocytes, oligodendrocytes, and microglia, actively participate in many complex functions within the CNS (immunity surveillance and inflammatory response, metabolic and synaptic homeostasis, modulation of blood-brain barrier—BBB) (Volterra and Meldolesi, 2005). [...]interaction with the elements of the extracellular matrix (ECM), an active player for long-term plasticity and circuit maintenance, adds another level of complexity to the modern model of the synapse structure (tetrapartite synapse) (Song and Dityatev, 2018). [...]if on one hand glial cells allow adaptive synaptic plasticity of CNS in several physiological conditions modulating synaptic transmission, homeostasis, and neural pathways signaling, then on the other, when activated, they boost inflammatory response and perturb neuroglial interactions, synaptic circuitry, and plasticity. Wei et al. hypothesized that mtROS/NLRP3 inflammasome may be part of the upstream pathway mediating the cleavage and release of the microglial interleukin 1 beta into brain areas including hippocampus that might play a pivotal role in POCD. Besides their role in neural circuitry and signaling, glial cells are also involved in axonal regeneration and nerve repair. The α7nAChR agonist PNU-282987 showed neuroprotective effects in astrocytes treated with 1-methyl-4-phenylpyridinium (MPP+), reducing the number of degenerating cells, and alleviating MPP -induced apoptosis. [...]PNU-282987 upregulated the expression of the antiapoptotic protein Bcl-2 and downregulated the expression of the apoptotic protein Bax and cleaved caspase-3, mainly via the JNK-p53-caspase-3 signaling (Hua et al.).