Inflammation in the Brain: Cellular Interactions, Molecular Pathways and Translation Toward Novel Therapies

Dear Colleagues,

Neuroinflammation represents a highly orchestrated biological response triggered in the central nervous system following brain injury, infection, or other insults. While initially aimed at restoring tissue homeostasis, this response involves a complex interplay among neurons, microglia, astrocytes, and endothelial cells. In its acute and controlled form, inflammation plays a beneficial role—facilitating pathogen clearance, promoting tissue repair, and supporting neurodevelopment. However, prolonged or dysregulated neuroinflammation is now recognized as a central driver of neurodegenerative processes. In conditions such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, chronic activation of immune signaling leads to persistent release of proinflammatory cytokines and chemokines. This, in turn, contributes to synaptic dysfunction, neuronal loss, and the progressive cognitive and motor decline characteristic of these disorders. Furthermore, evidence suggests that inflammation is not only a consequence of CNS disease development, but may also actively play a role at early stages of neurodegeneration. Indeed, neuroinflammation has emerged as one of the key hallmarks of neurodegeneration. This Special Issue invites contributions that explore the cellular and molecular crosstalk governing inflammatory responses in the brain. By illuminating the mechanisms that drive the shift from protective to chronic inflammation, this Issue aims to foster a deeper understanding of the molecular determinants of neurodegeneration and highlight innovative therapeutic strategies targeting neuroinflammatory pathways.

Prof. Dr. Maria Marino
Dr. Marco Fiocchetti
Dr. Evelyne Gozal
Guest Editors

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