PPubMed8 Apr 2020Cited 13×

Editorial: Neuroinflammation and Its Resolution: From Molecular Mechanisms to Therapeutic Perspectives

Morena Zusso, Leanne Stokes, Stefano Moro, Pietro Giusti

Abstract

Neuroinflammation, the complex immune response of the central nervous system (CNS), when sustained, is a common denominator in the etiology and course of all major neurological diseases, including neurodevelopmental, neurodegenerative, and psychiatric disorders (e.g., Alzheimer's disease, AD; Parkinson's disease, PD; multiple sclerosis, MS; motor neuron disease; depression; autism spectrum disorder; and schizophrenia). Cellular (microglia and mast cells, two brain-resident immune cells, together with astrocytes) and molecular immune components (e.g., cytokines, complement and pattern-recogniti

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The editorial summarizes 20 papers on neuroinflammation, highlighting mechanisms, disease links, and emerging therapeutic targets including plant‑derived compounds.

What’s new

i.Compilation of 20 original and review manuscripts covering neuroinflammation across multiple neurological disorders.
ii.Identification of novel therapeutic targets such as TRPM2, pleiotrophin‑midkine pathway, and microglial signaling molecules.
iii.Highlighting the potential of plant‑derived anti‑inflammatory compounds, reported in ~30% of the manuscripts.
iv.Emphasis on mechanisms of neuroinflammation resolution and drug development opportunities.

How they did it

The editors assembled and synthesized findings from 20 manuscripts, organized into five sections, providing a narrative overview of current research on neuroinflammation and its resolution.

What they found

TRPM2 knockout or inhibition markedly attenuated microglial activation in CNS disease models.
Dactolisib (dual PI3K/mTOR inhibitor) reduced social memory impairment and hippocampal IL‑10 levels in an AD mouse model after 14‑day oral treatment.
Scopoletin decreased disease severity, inflammation, and demyelination in experimental autoimmune encephalomyelitis mice via NF‑κB signaling.
Oridonin shifted macrophages toward anti‑inflammatory polarization and improved outcomes in experimental autoimmune neuritis.
GNF‑2, a Bcr‑Abl allosteric inhibitor, alleviated neuroinflammation‑associated pain in multiple animal pain models.
Simvastatin reduced neutrophil infiltration, brain edema, and pro‑inflammatory mediators after intracerebral hemorrhage in rats.
Approximately six manuscripts (~30% of the collection) investigated anti‑inflammatory effects of plant‑derived products.

Caveats

✕Development of small‑molecule drugs targeting microglia remains difficult due to their dynamic properties and CNS location.
✕Current antidepressants show adverse reactions, poor compliance, and high relapse risk, limiting their anti‑inflammatory utility.
✕Bicuculline reduced astrocytosis but failed to control overall glial activation in hyperammonemic rats.
✕High failure rate in translating neuroinflammation therapies to effective clinical treatments, especially for Alzheimer’s disease.

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