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Accelerated evolution of brain atrophy and “black holes” in MS patients with APOE ‐ε4
Author(s) -
Enzinger Christian,
Ropele Stefan,
Smith Stephen,
StrasserFuchs Siegrid,
Poltrum Birgit,
Schmidt Helena,
Matthews Paul M.,
Fazekas Franz
Publication year - 2004
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20027
Subject(s) - magnetic resonance imaging , apolipoprotein e , multiple sclerosis , atrophy , medicine , lesion , nuclear medicine , pathology , cardiology , gastroenterology , radiology , disease , immunology
Apolipoprotein E ( APOE )–ε4 has been associated with an unfavorable course of multiple sclerosis (MS). The mechanisms responsible for this are unclear, although cross‐sectional MRI demonstrated a higher extent of “black holes” (BHs) in such patients. Here, we have studied the impact of the APOE genotype on both the longitudinal evolution of focal (BH ratio) and global (brain volume change [BVC]) brain tissue damage. Ninety‐nine MS patients underwent ApoE genotyping, clinical examination, and magnetic resonance imaging at baseline and after 2.7 ± 1.1 years to assess lesion load (LL) and BVC. In APOE ‐ε4 patients, the annual reduction in brain volume was fivefold higher (−0.65 ± 0.61%) than in those without APOE ‐ε4 (−0.13 ± 0.36%; p = 0.0001). At baseline, T 2 LL and T 1 LL were non‐significantly higher in ε4 carriers, despite a shorter disease duration and absence of significant clinical differences. During follow‐up, T 1 LL increased from 1.2 ± 2.3ccm to 1.7 ± 2.7ccm in the ε4 group, although T 2 LL did not change, leading to a significantly higher increase in the BH ratio [(T 1 LL/T 2 LL) × 100] from 5.5 to 12.4% ( p = 0.005). BH ratio remained almost constant in non‐ε4 patients (5.0 vs 5.7%). Accelerated brain tissue loss and a higher proportion of lesions evolving into BH therefore provide magnetic resonance imaging evidence for more pronounced tissue destruction in MS patients with APOE ‐ε4. Ann Neurol 2004