tissue iron deposition and atrophy



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Doe

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<<snip>> Brain atrophy has also been related in cross-sectional and longitudinal studies to T2-
hypointense lesions in deep grey matter, suggesting a link between tissue iron deposition and
atrophy <<snip>>

Front Biosci. 2004 Jan 1;9:647-664. Related Articles, Links

Role of MRI in multiple sclerosis II: brain and spinal cord atrophy.

Zivadinov R, Bakshi R.

Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, 100 High St.,
Buffalo, NY 14203.

A growing body of evidence indicates that irreversible tissue destruction including axonal and
neuronal degeneration is a key component of the multiple sclerosis (MS) disease process. Magnetic
resonance imaging (MRI) is a powerful technique that can be combined with semiautomated or automated
computer assisted analysis approaches to detect progressive atrophy of the brain and spinal cord
with high sensitivity and reproducibility. The pathophysiology of central nervous system (CNS)
atrophy in MS is unknown but likely represents an epiphenomenon related to the effects of
inflammation including chronic demyelination, axonal injury, neuronal loss and Wallerian
degeneration. Other factors that may contribute to tissue atrophy include injury to the normal
appearing gray and white matter by mechanisms such as loss of growth factors, altered electrical
conduction and pathologic iron deposition. Prospective studies have suggested that atrophy in MS is
predicted by previous inflammatory activity as measured by overt MRI lesions. Gadolinium (Gd)-
enhancing lesions have shown a particularly strong predictive value in some but not all longitudinal
studies of brain atrophy. Brain atrophy has also been related in cross-sectional and longitudinal
studies to T2-hypointense lesions in deep grey matter, suggesting a link between tissue iron
deposition and atrophy. The measurement of brain atrophy seems to be of growing clinical relevance
as a biomarker of the MS disease process. Atrophy should now be included as a secondary endpoint in
trials of therapies aimed at limiting disease progression. Currently available anti-inflammatory
immunomodulatory agents and immunosuppressive treatments, while effective at preventing clinical
deterioration, have shown at best partial effects in preventing CNS atrophy. Thus, there is a need
to further validate atrophy as an outcome measure and ultimately develop treatment strategies that
will protect against the destructive aspects of the disease process. This should in turn lead to
better long term neurologic functioning and a better quality of life for patients with
MS.

PMID: 14766398 [PubMed - as supplied by publisher]

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