TY - JOUR
T1 - Toward Precision Phenotyping of Multiple Sclerosis
AU - Pitt, David
AU - Lo, Chih Hung
AU - Gauthier, Susan A.
AU - Hickman, Richard A.
AU - Longbrake, Erin
AU - Airas, Laura M.
AU - Mao-Draayer, Yang
AU - Riley, Claire
AU - De Jager, Philip Lawrence
AU - Wesley, Sarah
AU - Boster, Aaron
AU - Topalli, Ilir
AU - Bagnato, Francesca
AU - Mansoor, Mohammad
AU - Stuve, Olaf
AU - Kister, Ilya
AU - Pelletier, Daniel
AU - Stathopoulos, Panos
AU - Dutta, Ranjan
AU - Lincoln, Matthew R.
N1 - Publisher Copyright:
© 2022 American Academy of Neurology.
PY - 2022/11/30
Y1 - 2022/11/30
N2 - The classification of multiple sclerosis (MS) has been established by Lublin in 1996 and revised in 2013. The revision includes clinically isolated syndrome, relapsing-remitting, primary progressive and secondary progressive MS, and has added activity (i.e., formation of white matter lesions or clinical relapses) as a qualifier. This allows for the distinction between active and nonactive progression, which has been shown to be of clinical importance. We propose that a logical extension of this classification is the incorporation of additional key pathological processes, such as chronic perilesional inflammation, neuroaxonal degeneration, and remyelination. This will distinguish MS phenotypes that may present as clinically identical but are driven by different combinations of pathological processes. A more precise description of MS phenotypes will improve prognostication and personalized care as well as clinical trial design. Thus, our proposal provides an expanded framework for conceptualizing MS and for guiding development of biomarkers for monitoring activity along the main pathological axes in MS.
AB - The classification of multiple sclerosis (MS) has been established by Lublin in 1996 and revised in 2013. The revision includes clinically isolated syndrome, relapsing-remitting, primary progressive and secondary progressive MS, and has added activity (i.e., formation of white matter lesions or clinical relapses) as a qualifier. This allows for the distinction between active and nonactive progression, which has been shown to be of clinical importance. We propose that a logical extension of this classification is the incorporation of additional key pathological processes, such as chronic perilesional inflammation, neuroaxonal degeneration, and remyelination. This will distinguish MS phenotypes that may present as clinically identical but are driven by different combinations of pathological processes. A more precise description of MS phenotypes will improve prognostication and personalized care as well as clinical trial design. Thus, our proposal provides an expanded framework for conceptualizing MS and for guiding development of biomarkers for monitoring activity along the main pathological axes in MS.
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U2 - 10.1212/NXI.0000000000200025
DO - 10.1212/NXI.0000000000200025
M3 - Review article
C2 - 36041861
AN - SCOPUS:85136992193
SN - 2332-7812
VL - 9
JO - Neurology: Neuroimmunology and NeuroInflammation
JF - Neurology: Neuroimmunology and NeuroInflammation
IS - 6
M1 - e200025
ER -