Dying‐back oligodendrogliopathy: A late sequel of myelin‐associated glycoprotein deficiency

Ultrastructural analysis of myelin from 8‐month‐old mice deficient in the myelin‐associated glycoprotein revealed pronounced and characteristic alterations of the periaxonal oligodendrocyte processes, consisting of intracytoplasmic deposition of vesicular material, multivesicular bodies, mitochondria, and lipofuscin granules, as well as granular or paracrystalline inclusions. These alterations are similar to those described before as “dying‐back oligodendrogliopathy” in diseases of toxic or immune‐mediated demyelination including multiple sclerosis. © 1997 Wiley‐Liss Inc.

[1]  C. Godfraind,et al.  Expression of viral and myelin gene transcripts in a murine CNS demyelinating disease caused by a coronavirus , 2004, Glia.

[2]  R. Skoff,et al.  Programmed Cell Death in the Dysmyelinating Mutants , 1995, Brain pathology.

[3]  M. Schachner,et al.  Multiply myelinated axons in the optic nerve of mice deficient for the myelin‐associated glycoprotein , 1995, Glia.

[4]  M. Schachner,et al.  Crucial Role for the Myelin‐associated Glycoprotein in the Maintenance of Axon‐Myelin Integrity , 1995, The European journal of neuroscience.

[5]  K. Jellinger,et al.  Patterns of oligodendroglia pathology in multiple sclerosis. , 1994, Brain : a journal of neurology.

[6]  H. Lipp,et al.  Mice deficient for the glycoprotein show subtle abnormalities in myelin , 1994, Neuron.

[7]  J. Roder,et al.  Myelination in the absence of myelin-associated glycoprotein , 1994, Nature.

[8]  V. Friedrich,et al.  Many naturally occurring mutations of myelin proteolipid protein impair its intracellular transport , 1994, Journal of neuroscience research.

[9]  P. Lantos,et al.  The distribution of oligodendroglial inclusions in multiple system atrophy and its relevance to clinical symptomatology. , 1994, Brain : a journal of neurology.

[10]  Moses Rodriguez,et al.  Proteolipid Protein Gene Expression in Demyelination and Remyelination of the Central Nervous System: A Model for Multiple Sclerosis , 1994, Journal of neuropathology and experimental neurology.

[11]  C. Duyckaerts,et al.  Oligodendroglial and neuronal inclusions in multiple system atrophy , 1993, Current opinion in neurology.

[12]  P. Kelly,et al.  Oligodendrocyte injury is an early event in lesions of multiple sclerosis. , 1993, Mayo Clinic proceedings.

[13]  Moses Rodriguez Central nervous system demyelination and remyelination in multiple sclerosis and viral models of disease , 1992, Journal of Neuroimmunology.

[14]  P. Lantos,et al.  Accumulation of tubular structures in oligodendroglial and neuronal cells as the basic alteration in multiple system atrophy , 1992, Journal of the Neurological Sciences.

[15]  C. Brosnan,et al.  Cytokine cytotoxicity against oligodendrocytes. Apoptosis induced by lymphotoxin. , 1991, Journal of immunology.

[16]  P. Mcgeer,et al.  Oligodendroglial microtubular masses: An abnormality observed in some human neurodegenerative diseases , 1990, Neuroscience Letters.

[17]  M. K. Richards,et al.  The immune response to myelin proteolipid protein in the Lewis rat: identification of the immunodominant B cell epitope , 1990, Journal of Neuroimmunology.

[18]  H. Lassmann,et al.  Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein. , 1988, The American journal of pathology.

[19]  T. Fahrig,et al.  Myelin-associated glycoprotein, a member of the L2/HNK-1 family of neural cell adhesion molecules, is involved in neuron-oligodendrocyte and oligodendrocyte-oligodendrocyte interaction , 1987, The Journal of cell biology.

[20]  S. Ludwin,et al.  Evidence for a “dying‐back” gliopathy in demyelinating disease , 1981, Annals of neurology.

[21]  Ludwin Sk Chronic demyelination inhibits remyelination in the central nervous system. An analysis of contributing factors. , 1980 .

[22]  Y. Itoyama,et al.  Immunocytochemical observations on the distribution of myelin‐associated glycoprotein and myelin basic protein in multiple sclerosis lesions , 1980, Annals of neurology.

[23]  H. Wiśniewski,et al.  ULTRASTRUCTURAL STUDIES OF THE DYING‐BACK PROCESS: 1. PERIPHERAL NERVE TERMINAL AND AXON DEGENERATION IS SYSTEMIC ACRYLAMIDE INTOXICATION , 1974, Journal of neuropathology and experimental neurology.

[24]  B. Scheithauer,et al.  Ultrastructure of multiple sclerosis. , 1994, Ultrastructural pathology.