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Review
. 2019 Jan;148(2):168-187.
doi: 10.1111/jnc.14574. Epub 2018 Nov 12.

The S100B story: from biomarker to active factor in neural injury

Fabrizio Michetti  1   2 , Nadia D'Ambrosi  3 , Amelia Toesca  1 , Maria Ausiliatrice Puglisi  1 , Alessia Serrano  1 , Elisa Marchese  1 , Valentina Corvino  1 , Maria Concetta Geloso  1
Affiliations
Free article
Review

The S100B story: from biomarker to active factor in neural injury

Fabrizio Michetti et al. J Neurochem. 2019 Jan.
Free article

Abstract

S100B is a Ca2+ -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

Keywords: DAMP; S100B; biomarker; neuroinflammation.

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