The onset and progression of the lesion in multiple sclerosis☆
References (54)
- et al.
The morbid anatomy of the demyelinative diseases
Amer. J. Med.
(1952) - et al.
The cellular reaction to Wallerian degeneration in the CNS of the cat
Brain Res.
(1969) - et al.
Macrophages and cathepsin activity in multiple sclerosis brain
J. neurol. Sci.
(1974) The macrophage system, lipid metabolism and atherosclerosis
J. Atheroscler. Res.
(1964)- et al.
Degradation of encephalitogen by purified brain proteinase
FEBS Lett.
(1968) - et al.
Increased protease activity and changes in basic proteins and lipids in multiple sclerosis plaques
J. neurol. Sci.
(1970) Mechanism of demyelination in allergic encephalomyelitis in guinea pigs—An electron microscopic study
Exp. Neurol.
(1967)- et al.
An immune reaction in man against seminomas, dysgerminomas, pinealomas and the mediastinal tumours of similar histological appearance?
Lancet
(1964) The histochemistry of proteolytic enzymes and lipoproteins in the normal and diseased nervous system
Research on Multiple Sclerosis
(1972)
The demyelinative diseases of the human nervous system
Histochemistry of myelin, Part 2 (Proteins, lipid-protein dissociation and proteinase activity in Wallerian degeneration)
J. Neurochem.
Phagocytosis, lipid-removal and atherosclerosis
J. Path.
Histochemistry of myelin, Part 13 (Digestion of basic protein outside acute plaques of multiple sclerosis)
J. Neurochem.
Demyelination
Lysosomes in demyelination in the CNS white matter outside plaques
Europ. Neurol.
Cellular lipid inclusions in the white matter in multiple sclerosis
Nature (Lond.)
Biochemical studies of myelin in Wallerian degeneration of rat optic nerve
J. Neurochem.
A clinical and experimental contribution to the pathogenesis of disseminated sclerosis
Brain
Carboxypeptidases of human brain: Hydrolysis of benzyloxy-carbonyl-glubamyl-1-tyrosine in normal and diseased tissue
J. Neurochem.
The histology of disseminated sclerosis, Part 2 (Histological study)
Edinb. med. J., N.S.
The histology of disseminated sclerosis. Part 3 (Pathogenesis and etiology, a critical discussion)
Edinb. med. J., N.S.
Proteolytic activity and basic protein loss in and around multiple sclerosis plaques - Combined biochemical and histochemical observations
J. Neurochem.
Vessel-plaque relations, and cerebrospinal fluid and brain tissue changes in multiple sclerosis
Acta scand.
Enzyme histochemical studies in multiple sclerosis
Arch. Neurol. (Chic.)
Quantitative enzyme profiles of plaques of multiple sclerosis
Experientia
Observations on the histopathology of cerebral lesions in disseminated sclerosis
Brain
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The central vein sign is present in most infratentorial multiple sclerosis plaques
2022, Multiple Sclerosis and Related DisordersCitation Excerpt :Multiple sclerosis (MS) pathology studies have shown white matter lesions (WMLs) develop surrounding small veins (Adams, 1975).
Revealing vascular abnormalities and measuring small vessel density in multiple sclerosis lesions using USPIO
2021, NeuroImage: ClinicalCitation Excerpt :With the development of susceptibility-based venography in the late 1990s (Reichenbach et al., 1997), there has been a steady emphasis on the “central vein sign” or CVS hypothesis as a marker for and precursor to the development of new MS lesions (Gaitán et al., 2013; Maggi et al., 2015; Sati et al., 2016b; Tan et al., 2000). The perivascular space surrounding these veins is thought to be a privileged site for immune cells to interact with antigen-presenting cells, which can then trigger an inflammatory cascade leading to the formation of lesions around the veins (Adams, 1975; Barnett and Prineas, 2004). Studies have demonstrated that inflammation and injury to the blood–brain barrier of post-capillary venules enables the migration of blood constituents, including erythrocytes, lymphocytes, cytokines, glial cells etc.
Investigation of cerebral microbleeds in multiple sclerosis as a potential marker of blood-brain barrier dysfunction
2016, Multiple Sclerosis and Related DisordersCitation Excerpt :In MS, the situation appears to be different to those disorders with a primarily vascular pathology. Firstly histopathological studies demonstrate that in MS subcortical white matter lesions develop as a consequence of inflammation around small veins that drain into deep and superficial venous pathways (Adams, 1975; Fog, 1964), while the arterial vasculature does not seem to be affected. Secondly, structural changes of the vasculature have not been documented in MS patients.
Observations on the brain vasculature in multiple sclerosis: A historical perspective
2014, Multiple Sclerosis and Related DisordersCitation Excerpt :For example, McAlpine et al. in their 1955 textbook reviewed this literature extensively and concluded that ‘while the veins and venules have some influence in determining the sites of origin of the plaques they do not determine the subsequent evolution or form of the plaque and that thombosis, when it occurs, is a secondary process due to absorption of thromboplastic substance from the plaque’ (McAlpine et al., 1955). During the 1970s various authors confirmed the observation of a perivascular distribution of inflammation, and noted that this was more typical of the acute rather than chronic phase of the plaque (Adams, 1975; Guseo and Jellinger, 1975; Tanaka et al., 1975). Further work by Adams and colleagues documented perivenous iron deposition and other vascular damage in MS (Adams et al., 1985; Adams, 1988).
Optic neuritis: A mechanistic view
2011, PathophysiologyBacterial toxins and Multiple Sclerosis
2007, Journal of the Neurological Sciences
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This paper was read at the Symposium on Multiple Sclerosis, organized by the Medical Research Council and the Multiple Sclerosis Society, held in London on 17–18 October, 1974.