6533b834fe1ef96bd129cb8b

RESEARCH PRODUCT

Neurochemical and morphological studies on demyelination in multiple sclerosis with special reference to etiological aspects.

P.j. RiekkinenP.j. RiekkinenA.u. ArstilaA.u. ArstilaUrpo K. RinneUrpo K. Rinne

subject

Pathologymedicine.medical_specialtyMultiple SclerosisGlycoside HydrolasesBiopsyAcid PhosphataseBiologyInclusion bodiesMyelinNeurochemicalPhagocytosismedicineInner membraneHumansMyelin SheathGlucuronidaseCell NucleusInclusion BodiesMembranesMultiple sclerosisEsterasesLipid metabolismmedicine.diseaseLipid MetabolismAxonsPhosphoric Monoester HydrolasesCell nucleusMicroscopy Electronmedicine.anatomical_structureNeurologyNeurogliaNeurology (clinical)AutopsyLysosomesNeurogliaPeptide Hydrolases

description

Light microscopic studies were used as control for neurochemical studies and these showed that some micro plaques could be found also in areas which were normal on visual inspection. Also foreign cell infiltrates were found outside any clear plaque material. The number of these cells did not correlate with other findings like lipid or enzyme chemistry. In electronmicroscopic studies astrocytes demonstrated most lysosomes and phagocytosis of myelin. This increased lysosomal reaction was demonstrated also in biochemical analyses performed on MS biopsy specimens. Occasional nuclear changes like inclusion bodies and protrusion of inner nuclear membrane were observed suggesting some exogenous, possibly viral factor as an origin of the disease. Neurochemical studies showed that demyelination as a sense of decrease in myelin lipid and phosphohydrolase activity is only a later phenomenon and increased lysosomal activities possibly originating from various glial cells are found before demyelination. However myelin-like material found inside lysosomes suggests the early moderate demyelination before classical plaques can be found. Acid hydrolases were mostly increased at areas around plaques and encephalitogenic protein was not demonstrable at plaque areas. Our combined study suggests early changes of glial cells as a basic mechanism of the disease. However, the clarification of the basic course of these changes remains to be seen although nuclear changes may suggest a slow viral infection.

10.1007/bf00316038https://pubmed.ncbi.nlm.nih.gov/4120596