Showing papers by "Samuel K. Ludwin published in 1984"

Classic and generalized variants of Pick's disease: A clinicopathological, ultrastructural, and immunocytochemical comparative study

Abstract: Six sporadic cases of dementia with lobar atrophy and neuronal cytoplasmic inclusions (Pick's disease) could be separated into two groups on the basis of the involvement of subcortical structures, the distribution and the histochemical, immunochemical, and ultrastructural characteristics of the inclusions, and possibly the age at onset. The first group (classic) was characterized by predominantly cortical atrophy and the presence in the hippocampus and neocortex of argyrophilic cytoplasmic inclusion bodies that reacted with a monoclonal antibody against neurofilament proteins and antitubulin antisera. Ultrastructurally the bodies were composed of straight fibrils of variable diameter, averaging 15 nm, and long-period constricted fibrils. The second group (generalized) showed subcortical as well as cortical atrophy. Cortical and subcortical cytoplasmic inclusions contained RNA and stained poorly with silver and antibodies against neurofilaments and microtubules. Ultrastructurally the straight fibrils composing the bodies were coated with granular material, presumed to be derived from ribosomes. The generalized cases occurred in younger patients than did the classic cases in this series.

Proliferation of mature oligodendrocytes after trauma to the central nervous system.

Abstract: It has long been thought that mature oligodendrocytes in the adult mammalian central nervous system (CNS) are post-mitotic and are unable to proliferate in response to injury. The implications of this have been profound, because it has been suggested that this failure of oligodendrocytes to undergo mitosis is perhaps one of the reasons for the failure of the human CNS to undergo remyelination after demyelinating disease. This is in contrast with the normal peripheral nervous system in which there is consistent remyelination, and brisk Schwann cell mitosis. Although it has recently been shown that oligodendrocytes can be regenerated following some specific instances of demyelination, it has long been accepted that unlike mature astrocytes and microglia (macrophages), oligodendrocytes do not proliferate in response to general conditions damaging the nervous system. Here we show that mature oligodendrocytes in adult animals, as well as astrocytes and microglia, are able to respond to damage in the CNS following trauma by incorporating tritiated thymidine into their nuclei.

An immunohistochemical study of myelin proteins during remyelination in the central nervous system

Abstract: The process of remyelination in the superior cerebellar peduncles of mice following demyelination with Cuprizone was studied immunohistochemically using antisera to myelin basic protein (MBP) and myelin-associated glycoprotein (MAG). Demyelination occurred after formation of myelinic vacuoles and resulted in almost complete loss of demonstrable MBP and MAG from the peduncle. Prior to the onset of remyelination, oligodendrocytes with cytoplasmic staining for both proteins appeared in the peduncle. These cells were then associated with remyelinating axons. The axons were remyelinated in clusters until the MBP and the MAG in the whole peduncle were reconstituted, although the axon sheaths were thinner than those in normal animals. The results show that the immunohistochemical distribution of MBP and MAG in remyelinating axons resembles that in normal axons, and that the expression of myelin proteins in oligodendrocytes during remyelination reverts to that seen during normal development.