Chapter 10 

 DEMYELINATION 



W, 



e offer no apology for including a discussion of the myelin 

 sheath of nerve fibres in our programme, for it is very frequently the 

 site of serious damage that cannot be separated from the nerve and 

 neuroglial cells whose existence is so closely linked with the pre- 

 servation of that sheath. Demyelinating diseases still offer the 

 supreme challenge to the neurologist; they afford the investigator 

 a unique opportunity for exact chemical study of a unique cellular 

 function. 



Electron microscopic and x-ray diffraction studies show the 

 myelin sheath to be a highly organised structure in which an 

 orientated double layer of lipid alternates with a protein layer 

 (Schmitt, 1939; Schmitt and Palmer, 1941) . Cholesterol is an in- 

 tegral part of this lipoprotein complex (Fernandez-Moran and 

 Finean, 1957) . The sheath is made up of a number of lamellae each 

 about 140 Angstrom units wide and varying from one or two in 

 "unmyelinated" nerve to thirty-six or more layers in the myelinated 

 nerve. Modern investigations have established an intimate relation- 

 ship between the myelin and the Schwann cells that are grouped 

 about the peripheral axons. It appears that the lamellae of myelin 

 are wound around the axon layer by layer, like a bandage, the ends 

 remaining attached on the inside to the axolemma and on the out- 

 side to the Schwann cell membrane (Lumsden, 1957) . There is 

 little doubt that the Schwann cell is responsible for this winding 

 process but how it does it is still debated. Confirmation has come 

 from the tissue culture studies of Peterson and Murray (1955) who 

 have adroitly followed myelination in vitro though they could not 

 decide whether lipid comes from the axon proper or the Schwann 

 membrane. A similar mechanism quite likely holds between the 

 oligodendrocytes and the axons of the central nervous system. 



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