Abstract Volume 22 Issue 2 (2001) pp 141-144
I. V. Allen (1), S. McQuaid (2), M. Mirakhur (2), G. Nevin (3)
(1) School of Biology and Biochemistry, Medical Biology Centre, Queen's University of Belfast, Lisburn Road, Belfast BT9 7BL, Northern Ireland, UK
(2) Regional Neuropathology Laboratory, Royal Group of Hospitals Trust, Belfast, Northern Ireland, UK
(3) School of Biomedical Sciences, University of Ulster, Ulster, Northern Ireland, UK
In established cases of multiple sclerosis (MS), the normal-appearing white matter (NAWM), as defined for magnetic resonance imaging (MRI), is abnormal in the majority of cases.
The clinical significance of these NAWM abnormalities is the subject of debate, but there is strong correlation with degree and progression of disability.
New lesions form in NAWM before blood-brain barrier breakdown, as evidenced by gadolinium enhancement.
The pathological basis of these neuroimaging abnormalities is largely unknown.
Definitive pathological studies on the NAWM are few and are often based on small numbers of samples and of cases.
Despite a variety of MS NAWM pathological studies, major research questions, of importance to our understanding of basic pathogenetic mechanisms and consequent rational therapies, remain unanswered.
These relate to the frequency and extent of oligodendrocyte/myelin and axonal abnormalities in MS NAWM, and to the cellular basis of very early MS lesions detected by neuroimaging.
In a pilot study of MS NAWM, microglial activation was demonstrated in 9 of 10 MS cases.
We are currently testing the hypothesis
that microglial activation, as defined by altered phenotype and HLA-DR
positivity, will act as a marker for oligodendrocyte/myelin and axonal
pathology in MS NAWM.
© Springer-Verlag Italia 2001