TY - JOUR
T1 - Modulating acute neuroinflammation in intracerebral hemorrhage
T2 - the potential promise of currently approved medications for multiple sclerosis
AU - Napier, Jarred
AU - Rose, Lucas
AU - Adeoye, Opeolu
AU - Hooker, Edmond
AU - Walsh, Kyle B.
N1 - Publisher Copyright:
© 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.
PY - 2019/1/2
Y1 - 2019/1/2
N2 - The secondary inflammatory injury following intracerebral hemorrhage (ICH) results in increased morbidity and mortality. White blood cells have been implicated as critical mediators of this inflammatory injury. Currently, no medications have been clinically proven to ameliorate or beneficially modulate inflammation, or to improve outcomes by any mechanism, following ICH. However, other neuroinflammatory conditions, such as multiple sclerosis, have approved pharmacologic therapies that modulate the inflammatory response and minimize the damage caused by inflammatory cells. Thus, there is substantial interest in existing therapies for neuroinflammation and their potential applicability to other acute neurological diseases such as ICH. In this review, we examined the mechanism of action of twelve currently approved medications for multiple sclerosis: alemtuzumab, daclizumab, dimethyl fumarate, fingolimod, glatiramer acetate, interferon beta-1a, interferon beta-1b, mitoxantrone, natalizumab, ocrelizumab, rituximab, teriflunomide. We analyzed the existing literature pertaining to the effects of these medications on various leukocytes and also with emphasis on mechanisms of action during the acute period following initiation of therapy. As a result, we provide a valuable summary of the current body of knowledge regarding these therapies and evidence that supports or refutes their likely promise for treating neuroinflammation following ICH.
AB - The secondary inflammatory injury following intracerebral hemorrhage (ICH) results in increased morbidity and mortality. White blood cells have been implicated as critical mediators of this inflammatory injury. Currently, no medications have been clinically proven to ameliorate or beneficially modulate inflammation, or to improve outcomes by any mechanism, following ICH. However, other neuroinflammatory conditions, such as multiple sclerosis, have approved pharmacologic therapies that modulate the inflammatory response and minimize the damage caused by inflammatory cells. Thus, there is substantial interest in existing therapies for neuroinflammation and their potential applicability to other acute neurological diseases such as ICH. In this review, we examined the mechanism of action of twelve currently approved medications for multiple sclerosis: alemtuzumab, daclizumab, dimethyl fumarate, fingolimod, glatiramer acetate, interferon beta-1a, interferon beta-1b, mitoxantrone, natalizumab, ocrelizumab, rituximab, teriflunomide. We analyzed the existing literature pertaining to the effects of these medications on various leukocytes and also with emphasis on mechanisms of action during the acute period following initiation of therapy. As a result, we provide a valuable summary of the current body of knowledge regarding these therapies and evidence that supports or refutes their likely promise for treating neuroinflammation following ICH.
KW - Intracerebral hemorrhage
KW - immunomodulation
KW - multiple sclerosis
KW - neuroinflammation
UR - http://www.scopus.com/inward/record.url?scp=85066058332&partnerID=8YFLogxK
U2 - 10.1080/08923973.2019.1566361
DO - 10.1080/08923973.2019.1566361
M3 - Review article
C2 - 30702002
AN - SCOPUS:85066058332
VL - 41
SP - 7
EP - 15
JO - Immunopharmacology and Immunotoxicology
JF - Immunopharmacology and Immunotoxicology
SN - 0892-3973
IS - 1
ER -