Axonal Pathology in Multiple Sclerosis. A Historical Note

Kornek, Barbara; Lassmann, Hans

doi:10.1111/j.1750-3639.1999.tb00547.x

Cited by 186 publications

(92 citation statements)

References 48 publications

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“…This stands in interesting contrast to our existing demonstration of a loss of myelin [3]. The demonstration of relative (if not complete) axonal preservation in the context of myelin loss clearly has parallels with multiple sclerosis [6]. In this context it is interesting that microarray studies have demonstrated that both deep subcortical lesions [7] and multiple sclerosis plaques [8] occur against background field changes in the socalled 'normal appearing white matter' .…”

Section: Discussioncontrasting

confidence: 51%

Axonal Preservation in Deep Subcortical White Matter Lesions in the Ageing Brain

Highley¹,

Gebril²,

Simpson³

et al. 2014

Aging Sci

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Cerebral white matters lesions (WML) are seen in 94% of the population aged 64 and over and are associated with cognitive decline and depression. We used immunohistochemistry and stereological methods on post mortem brain samples derived from the Medical Research Council Cognitive Function and Ageing Study (MRC-CFAS) cohort to investigate the axonal density within deep subcortical lesions. There was no significant difference between the lesional and control white matter, therefore, we conclude that there is axonal preservation within these lesions that are characterized by demyelination.

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Section: Discussioncontrasting

confidence: 51%

Axonal Preservation in Deep Subcortical White Matter Lesions in the Ageing Brain

Highley¹,

Gebril²,

Simpson³

et al. 2014

Aging Sci

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“…This result is in agreement with studies in MS patients and MOGinduced chronic EAE in Lewis rats in which axonal APP staining was most pronounced in actively demyelinating plaques (40). Axonal damage as a consequence of demyelination or dysmyelination is a common finding (41), and axonal loss was described in the first observations of MS (42). The role of axonal damage in the pathology of MS has undergone a resurgence of interest.…”

Section: Discussionmentioning

confidence: 99%

The Membrane Attack Complex of Complement Causes Severe Demyelination Associated with Acute Axonal Injury

Mead¹,

Singhrao²,

Neal

et al. 2002

The Journal of Immunology

183

131

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Complement is implicated in pathology in the human demyelinating disease multiple sclerosis and in animal models that mimic the demyelination seen in multiple sclerosis. However, the components of the complement system responsible for demyelination in vivo remain unidentified. In this study, we show that C6-deficient (C6−) PVG/c rats, unable to form the membrane attack complex (MAC), exhibit no demyelination and significantly reduced clinical score in the Ab-mediated experimental autoimmune encephalomyelitis model when compared with matched C6-sufficient (C6+) rats. In C6+ rats, perivenous demyelination appeared, accompanied by abundant mononuclear cell infiltration and axonal injury. Neither demyelination nor axonal damage was seen in C6− rats, whereas levels of mononuclear cell infiltration were equivalent to those seen in C6+ rats. Reconstitution of C6 to C6− rats yielded pathology and clinical disease indistinguishable from that in C6+ rats. We conclude that demyelination and axonal damage occur in the presence of Ab and require activation of the entire complement cascade, including MAC deposition. In the absence of MAC deposition, complement activation leading to opsonization and generation of the anaphylatoxins C5a and C3a is insufficient to initiate demyelination.

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“…Symptoms are associated with a pathogenic CNS-targeted autoimmune response sustained by leukocytes that invade brain and spinal cord parenchyma and accumulate in multifocal sclerotic plaques, the pathological hallmark of MS from which the disease gets its name [126]. After CNS entry, immune cells destroy myelin and oligodendrocytes and lead to axon degeneration and neuron loss.…”

Section: Multiple Sclerosis and Neuroinflammationmentioning

confidence: 99%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

278

206

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a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

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Axonal Pathology in Multiple Sclerosis. A Historical Note

Cited by 186 publications

References 48 publications

Axonal Preservation in Deep Subcortical White Matter Lesions in the Ageing Brain

Axonal Preservation in Deep Subcortical White Matter Lesions in the Ageing Brain

The Membrane Attack Complex of Complement Causes Severe Demyelination Associated with Acute Axonal Injury

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

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