About this Research Topic

Background

Historically thought to play a passive role supporting neurons in the central nervous system, glial cells have emerged as vital players that function to actively maintain the health of neurons. Unfortunately, the same critical functions that glial cells execute in promoting neuronal health can become maladaptive when they are altered in the context of disease. A significant body of literature now indicates that glial cells can actively contribute to disease pathogenesis in a number of different neuroinflammatory and neurodegenerative diseases of the human central nervous system. A discussion of these emerging pathological mechanisms and translational strategies for bringing novel therapeutics targeting them into clinical development would be both timely and of high value to the field.

Emerging human biology data (e.g. genetics) indicate that glia contribute to CNS disease pathogenesis and are yielding promising new therapeutic targets. There is an urgent need to develop novel therapeutics against the most promising of these targets. However, the preclinical path to developing such therapeutics and successfully translating them to clinical study remains marked with challenges. In particular, animal models of neuroinflammatory and neurodegenerative CNS disease have been developed, but species differences in immunology (e.g. rodent vs. human) pose significant challenges for understanding disease mechanisms and translating novel therapies. Additionally, challenges remain in identifying in vitro systems predictive of in vivo glial cell response. In vivo approaches must further account for the confounding effects that anesthesia can have on CNS glial cell function. Furthermore, many studies of novel therapeutics rely on acute dosing and the rescue of pharmacodynamic endpoints unrelated to disease pathogenesis, rather than also pursuing chronic dosing and endpoints that reflect disease pathogenesis. For studies of age-related diseases (e.g. AD), relatively few studies evaluate therapeutic effects in aged animals. Finally, novel biomarkers (e.g. PET, fluid) are urgently needed to both facilitate the study of human disease mechanism and translate novel therapies to the clinic. Current strategies (e.g. TSPO PET) are limited and such advances will help enable patient stratification for studying CNS diseases involving glial pathogenesis.

This collection focuses on the preclinical development and clinical translation of novel therapeutics targeting glial cell mechanisms to treat CNS disease. All phases of preclinical development, from target identification and validation, through clinical translational studies are in-scope. Three core themes are emphasized:

1) Novel therapeutic development for neurodegenerative and neuroinflammatory CNS diseases

• Scope: Articles focusing on novel therapeutic development against targets motivated by human biology data (e.g. genetics) are of particular interest in the areas of neurodegenerative and neuroinflammatory CNS diseases (both neurologic and psychiatric).

2) Influence of novel glial therapeutics and targets on neuronal function and structure

• Scope: both direct and indirect effects of glial drug targets on neuronal function and structure in vitro and in vivo are of interest.

3) Clinical translation strategies for glia-targeted therapeutics

• Scope: biomarkers and functional endpoints for assessing novel glia-targeted therapeutics for neurodegenerative and neuroinflammatory CNS diseases. Those with clinical utility are of particular interest, including: target engagement, pharmacodynamic, efficacy, and patient stratification biomarkers.

Topic Editor Dr. Evan Lebois licensed technology to Acadia Pharmaceuticals for which he has received licensing revenue. Topic Editor Dr. Justin Piro is employed by Alkermes, Plc. Topic Editor Prof. Malú Tansey is co-inventor of XPro1595 (pegipanermin). The other Topic Editors declare no competing conflicts of interest.

Keywords: Glia, Neuroinflammation, Neurodegeneration, Therapeutics, Translation

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