Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients

By Ranjan Dutta, J. McDonough, Xinghua Yin, J. Peterson, Ansi Chang, T. Torres, T. Gudz, W. Macklin, D. Lewis, R. Fox and 3 more. Annals of Neurology, 2006

862 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/bbcfcc890b18c77905ae74fcffebb638fb647092

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In Developmental Neuroscience

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Citations in the corpus

A Gradient of neuronal loss and meningeal inflammation in multiple sclerosis (2010, background): “At present, it is unclear how extensive these neuronal changes are and whether they represent primary neuronal damage or are occurring as a result of downstream WM lesions.(9,11,12) The lack of inflammatory cell infiltrates and foamy macrophages and scarce deposition of immunoglobulin (Ig) and compl”
Oxidative damage in multiple sclerosis lesions (2011, background): “…may contribute to demye- lination and neurodegeneration in multiple sclerosis, it recently became clear that mitochondrial injury and subsequent energy failure is a major factor driving tissue injury (Lu et al., 2000; Dutta et al., 2006; Mahad et al., 2008; Trapp and Stys 2009; Witte et al., 2010).”
A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis (2011, result): “Our findings provide a mechanistic framework for recent histopathological studies that showed damage to neuronal mitochondria in acute and chronic stages of multiple sclerosi”
Remyelination in the CNS: from biology to therapy (2008, background): “This in turn will activate intra-axonal proteases, resulting in neurofilament fragmentation and perturbation of axon transport and integrit”
The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “Another microarray investigation revealed a decreased expression of genes involved in mitochondrial energy metabolism (26).”
The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “…to remyelination due to intrinsic axolemmal changes, possibly including expression of inhibitory cell surface molecules such as polysialylated-neural cell adhesion molecule (Charles et al., 2000), changes in membrane caliber, neurofilament fragmentation, or energy failure (Dutta et al., 2006).”
Multiple Sclerosis Pathology. (2018, background): “This process is associated with mitochondrial damage reflected by the presence of respiratory-deficient cells and the accumulation of mitochondrial gene deletions (Dutta et al. 2006; Mahad et al. 2008; Campbell et al. 2011).”