Plasma levels of neuron specific enolase quantify the extent of neuronal injury in murine models of ischemic stroke and multiple sclerosis.
OBJECTIVE
We aimed at validating a plasma biomarker for neuronal damage that can be used in acute and chronic models of neurological diseases.


METHODS
We investigated two different models, middle cerebral artery occlusion followed by reperfusion and MOG35-55-induced experimental autoimmune encephalomyelitis (EAE). In stroke experiments we measured infarct sizes by magnetic resonance imaging and vital stainings and correlated them with plasma levels of neuron specific enolase (NSE) at different time points after reperfusion. Equally, in EAE experiments, we correlated NSE levels with neurological scores and histopathological damage of axons at different time points. We detected plasma NSE levels by ELISA.


RESULTS
Plasma NSE levels correlated significantly with stroke size, EAE score and histopathological damage in EAE. Investigations into the dynamics of neuronal loss over time correlated well with the dynamics of NSE levels. NSE even predicted the onset of EAE, before clinical signs were recordable.


CONCLUSIONS
Plasma NSE is a valid and simple experimental biomarker that allows quantifying the degree of neuronal injury in a non-invasive approach.
Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Mathias
M
Gelderblom
Tristan
T
Daehn
Benjamin
B
Schattling
Peter
P
Ludewig
Christian
C
Bernreuther
Priyadharshini
P
Arunachalam
Jakob
J
Matschke
Markus
M
Glatzel
Christian
C
Gerloff
Manuel A
MA
Friese
Tim
T
Magnus
D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000166:cytology; D020520:Brain Infarction / Q000209:etiology / Q000473:pathology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004622:Embryo, Mammalian; D018698:Glutamic Acid / Q000633:toxicity; D020244:Infarction, Middle Cerebral Artery / Q000097:blood* / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D051379:Mice; D008810:Mice, Inbred C57BL; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009103:Multiple Sclerosis / Q000097:blood* / Q000139:chemically induced / Q000473:pathology*; D063308:Myelin-Oligodendrocyte Glycoprotein / Q000633:toxicity; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D010446:Peptide Fragments / Q000633:toxicity; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D013997:Time Factors
D016564:Amyloid beta-Protein Precursor; D008869:Microtubule-Associated Proteins; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; C445081:myelin oligodendrocyte glycoprotein (35-55); D018698:Glutamic Acid; D007770:L-Lactate Dehydrogenase; D010751:Phosphopyruvate Hydratase
MOG(35–55)-induced experimental autoimmune encephalomyelitis (EAE); Middle cerebral artery occlusion; Neurological disease; Neuron specific enolase (NSE); Neuronal damage; Plasma biomarker; Stroke