Open AccessRESEARCH ARTICLE: Myelin Abnormalities without Oligodendrocyte Loss in Periventricular Leukomalacia
Author(s) -
Billiards Saraid S.,
Haynes Robin L.,
Folkerth Rebecca D.,
Borenstein Natalia S.,
Trachtenberg Felicia L.,
Rowitch David H.,
Ligon Keith L.,
Volpe Joseph J.,
Kinney Hannah C.
Publication year - 2008
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2007.00107.x
Subject(s) - immunostaining , olig2 , periventricular leukomalacia , oligodendrocyte , myelin basic protein , myelin , pathology , lineage markers , white matter , context (archaeology) , immunohistochemistry , biology , medicine , neuroscience , magnetic resonance imaging , microbiology and biotechnology , central nervous system , gestational age , pregnancy , paleontology , progenitor cell , genetics , stem cell , radiology
The cellular basis of myelin deficits detected by neuroimaging in long‐term survivors of periventricular leukomalacia (PVL) is poorly understood. We tested the hypothesis that oligodendrocyte lineage (OL) cell density is reduced in PVL, thereby contributing to subsequent myelin deficits. Using computer‐based methods, we determined OL cell density in sections from 18 PVL and 18 age‐adjusted control cases, immunostained with the OL‐lineage marker Olig2. Myelination was assessed with myelin basic protein (MBP) immunostaining. We found no significant difference between PVL and control cases in Olig2 cell density in the periventricular or intragyral white matter. We did find, however, a significant increase in Olig2 cell density at the necrotic foci, compared with distant areas. Although no significant difference was found in the degree of MBP immunostaining, we observed qualitative abnormalities of MBP immunostaining in both the diffuse and necrotic components of PVL. Abnormal MBP immunostaining in PVL despite preserved Olig2 cell density may be secondary to arrested OL maturation, damage to OL processes, and/or impaired axonal‐OL signaling. OL migration toward the “core” of injury may occur to replenish OL cell number. This study provides new insight into the cellular basis of the myelin deficits observed in survivors of PVL.