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The S100B story: from biomarker to active factor in neural injury
Author(s) -
Michetti Fabrizio,
D'Ambrosi Nadia,
Toesca Amelia,
Puglisi Maria Ausiliatrice,
Serrano Alessia,
Marchese Elisa,
Corvino Valentina,
Geloso Maria Concetta
Publication year - 2019
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.14574
Subject(s) - biomarker , medicine , multiple sclerosis , disease , mood disorders , traumatic brain injury , schizophrenia (object oriented programming) , stroke (engine) , brain damage , amyotrophic lateral sclerosis , bioinformatics , pathology , immunology , psychiatry , biology , mechanical engineering , anxiety , biochemistry , engineering
S100B is a Ca 2+ ‐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.