Axon pathology in neurological disease: A neglected therapeutic target

Trends in Neurosciences

Volumn 25, Issue 10, 2002, Pages 532-537

  Coleman, Michael P ^a   Perry, V Hugh ^b  

^a UNIVERSITY OF COLOGNE   (Germany)

^b UNIVERSITY OF SOUTHAMPTON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

3,3' IMINODIPROPIONITRILE; ACETONYLACETONE; AMYLOID BETA PROTEIN; CISPLATIN; NICOTINAMIDE ADENINE DINUCLEOTIDE; NICOTINAMIDE NUCLEOTIDE ADENYLYLTRANSFERASE; PACLITAXEL; PROTEASOME; PROTEIN; PROTEIN UBE4B; UBIQUITIN; UNCLASSIFIED DRUG; VINCRISTINE;

AMINO TERMINAL SEQUENCE; APOPTOSIS; BRAIN INJURY; CARBOXY TERMINAL SEQUENCE; CELL LOSS; CYTOPATHOLOGY; HUMAN; MULTIPLE SCLEROSIS; MUTATION; MYELINATION; NERVE DEGENERATION; NERVE FIBER DEGENERATION; NERVE FIBER TRANSPORT; NEUROLOGIC DISEASE; NEUROPROTECTION; NONHUMAN; OXYGENATION; PATHOGENESIS; PERIPHERAL NEUROPATHY; PRIORITY JOURNAL; PROTEIN EXPRESSION; REGULATORY MECHANISM; REVIEW; SPINAL CORD INJURY; STROKE; SYNAPSE;

ANIMALS; AXONS; CYSTEINE ENDOPEPTIDASES; HUMANS; MULTIENZYME COMPLEXES; MUTATION; NERVE DEGENERATION; NERVE TISSUE PROTEINS; NERVOUS SYSTEM DISEASES; PROTEASOME ENDOPEPTIDASE COMPLEX; UBIQUITIN;

EID: 0036774951     PISSN: 01662236     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0166-2236(02)02255-5     Document Type: Review

References (74)

1. Frahm H.D., et al. Comparison of brain structure volumes in Insectivora and Primates. I. Neocortex. J. Hirnforsch. 23:1982;375-389.
2. De Keyser J., et al. Clinical trials with neuroprotective drugs in acute ischaemic stroke: are we doing the right thing? Trends Neurosci. 22:1999;535-540.
3. Deckwerth T.L., Johnson E.M. Jr. Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis). Dev. Biol. 165:1994;63-72.
4. Sagot Y., et al. Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease. J. Neurosci. 15:1995;7727-7733.
5. Finn J.T., et al. Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation Do not involve caspases. J. Neurosci. 20:2000;1333-1341.
6. Lunn E.R., et al. Absence of Wallerian degeneration does not hinder regeneration in peripheral nerve. Eur. J. Neurosci. 1:1989;27-33.
7. Mack T.G., et al. Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene. Nat. Neurosci. 4:2001;1199-1206.
8. S protein protects against axonal degeneration: a model of gene therapy for peripheral neuropathy. Ann. Neurol. 50:2001;773-779.
9. Waller A.V. Experiments on the section of glossopharyngeal and hypoglossal nerves of the frog, and observations on the alterations produced thereby in the structure of their primitive fibres. Philos. Trans. R. Soc. Lond. B Biol. Sci. 140:1850;423-429.
10. Cliffer K.D., et al. Physiological characterization of Taxol-induced large-fiber sensory neuropathy in the rat. Ann. Neurol. 43:1998;46-55.
11. Frei R., et al. Loss of distal axons and sensory Merkel cells and features indicative of muscle denervation in hindlimbs of P0-deficient mice. J. Neurosci. 19:1999;6058-6067.
12. Garbern J.Y., et al. Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation. Brain. 125:2002;551-561.
13. Probst A., et al. Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein. Acta Neuropathol. 99:2000;469-481.
14. Oosthuyse B., et al. Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration. Nat. Genet. 28:2001;131-138.
15. Saigoh K., et al. Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice. Nat. Genet. 23:1999;47-51.
16. Cifuentes-Diaz C., et al. Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse model. Hum. Mol. Genet. 11:2002;1439-1447.
17. Schlaepfer W.W., Hasler M.B. Characterization of the calcium-induced disruption of neurofilaments in rat peripheral nerve. Brain Res. 168:1979;299-309.
18. + levels. Eur. J. Neurosci. 7:1995;1596-1602.
19. Glass J.D., et al. Prolonged survival of transected nerve fibres in C57BL/Ola mice is an intrinsic characteristic of the axon. J. Neurocytol. 22:1993;311-321.
20. Perry V.H., et al. Evidence that very slow Wallerian degeneration in C57BL/Ola mice is an intrinsic property of the peripheral nerve. Eur. J. Neurosci. 2:1990;802-808.
21. Perry V.H., et al. Very slow retrograde and Wallerian degeneration in the CNS of C57BL/Ola mice. Eur. J. Neurosci. 3:1991;102-105.
22. Steward O. Signals that induce sprouting in the central nervous system: sprouting is delayed in a strain of mouse exhibiting delayed axonal degeneration. Exp. Neurol. 118:1992;340-351.
23. Perry V.H., et al. Evidence that the rate of Wallerian degeneration is controlled by a single autosomal dominant gene. Eur. J. Neurosci. 2:1990;408-413.
24. S). Eur. J. Neurosci. 9:1997;1586-1592.
25. S mutant and Ube4b/Nmnat transgenic mice. J. Physiol. (in press)
26. Lyon M.F., et al. A gene affecting Wallerian nerve degeneration maps distally on mouse chromosome 4. Proc. Natl. Acad. Sci. U. S. A. 90:1993;9717-9720.
27. S) mouse. Proc. Natl. Acad. Sci. U. S. A. 95:1998;9985-9990.
28. S) mouse. Proc. Natl. Acad. Sci. U. S. A. 97:2000;11377-11382.
29. Emanuelli M., et al. Molecular cloning, chromosomal localization, tissue mRNA levels, bacterial expression, and enzymatic properties of human NMN adenylyltransferase. J. Biol. Chem. 276:2001;406-412.
30. S) mouse. Gene. 284:2002;23-29.
31. Mukoyama M., et al. Neuropathology of the gracile axonal dystrophy (gad) mouse. Acta Neuropathol. 79:1989;294-299.
32. Kent C., Clarke P.J. The immunolocalisation of the neuroendocrine specific protein PGP9.5 during neurogenesis in the rat. Brain Res. Dev. Brain Res. 58:1991;147-150.
33. Shimura H., et al. Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase. Nat. Genet. 25:2000;302-305.
34. Lowe J., et al. Ubiquitin in neurodegenerative diseases. Brain Pathol. 3:1993;55-65.
35. Layfield R., et al. The ubiquitin protein catabolic disorders. Neuropathol. Appl. Neurobiol. 27:2001;171-179.
36. Koegl M., et al. A novel ubiquitination factor, E4, is involved in multiubiquitin chain assembly. Cell. 96:1999;635-644.
37. Hatakeyama S., et al. U-Box proteins as a new family of ubiquitin-protein ligases. J. Biol. Chem. 276:2001;33111-33120.
38. Lam Y.A., et al. Inhibition of the ubiquitin-proteasome system in Alzheimer's disease. Proc. Natl. Acad. Sci. U. S. A. 97:2000;9902-9906.
39. Mahoney J.A., et al. The human homologue of the yeast polyubiquitination factor Ufd2p is cleaved by caspase 6 and granzyme B during apoptosis. Biochem. J. 361:2002;587-595.
40. Buki A., et al. Cytochrome c release and caspase activation in traumatic axonal injury. J. Neurosci. 20:2000;2825-2834.
41. Ivins K.J., et al. Beta-amyloid induces local neurite degeneration in cultured hippocampal neurons: evidence for neuritic apoptosis. Neurobiol. Dis. 5:1998;365-378.
42. Bodine S.C., et al. Identification of ubiquitin ligases required for skeletal muscle atrophy. Science. 294:2001;1704-1708.
43. Kornek B., Lassmann H. Axonal pathology in multiple sclerosis. A historical note. Brain Pathol. 9:1999;651-656.
44. Kandel E.R., et al. Principles of Neural Science. 2000;McGraw-Hill.
45. Narayanan S., et al. Imaging of axonal damage in multiple sclerosis: spatial distribution of magnetic resonance imaging lesions. Ann. Neurol. 41:1997;385-391.
46. Sherriff F.E. Early detection of axonal injury after human head trauma using immunocytochemistry for β-amyloid precursor protein. Acta Neuropathol. Berl. 87:1994;55-62.
47. Ferguson B., et al. Axonal damage in acute multiple sclerosis lesions. Brain. 120:1997;393-399.
48. Trapp B.D. Axonal transection in the lesions of multiple sclerosis. N. Engl. J. Med. 338:1998;278-285.
49. Evangelou N., et al. Regional axonal loss in the corpus callosum correlates with cerebral white matter lesion volume and distribution in multiple sclerosis. Brain. 123:2000;1845-1849.
50. Evangelou N., et al. Size-selective neuronal changes in the anterior optic pathways suggest a differential susceptibility to injury in multiple sclerosis. Brain. 124:2001;1813-1820.
51. Bjartmar C., Trapp B.D. Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences. Curr. Opin. Neurol. 14:2001;271-278.
52. Gurney M.E., et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. Science. 264:1994;1772-1775.
53. Bordet T., et al. Protective effects of cardiotrophin-1 adenoviral gene transfer on neuromuscular degeneration in transgenic ALS mice. Hum. Mol. Genet. 10:2001;1925-1933.
54. Sagot Y., et al. An orally active anti-apoptotic molecule (CGP 3466B) preserves mitochondria and enhances survival in an animal model of motoneuron disease. Br. J. Pharmacol. 131:2000;721-728.
55. Xu Z., et al. Increased expression of neurofilament subunit NF-L produces morphological alterations that resemble the pathology of human motor neuron disease. Cell. 73:1993;23-33.
56. Al-Chalabi A., et al. Deletions of the heavy neurofilament subunit tail in amyotrophic lateral sclerosis. Hum. Mol. Genet. 8:1999;157-164.
57. Warita H., et al. Selective impairment of fast anterograde axonal transport in the peripheral nerves of asymptomatic transgenic mice with a G93A mutant SOD1 gene. Brain Res. 819:1999;120-131.
58. Williamson T.L., Cleveland D.W. Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons. Nat. Neurosci. 2:1999;50-56.
59. Kennel P.F., et al. Neuromuscular function impairment is not caused by motor neurone loss in FALS mice: an electromyographic study. Neuroreport. 7:1996;1427-1431.
60. Hirokawa N. Kinesin and dynein superfamily proteins and the mechanism of organelle transport. Science. 279:1998;519-526.
61. Zhao C., et al. Charcot-Marie-Tooth disease type 2A caused by mutation in a microtubule motor KIF1Bbeta. Cell. 105:2001;587-597.
62. LaMonte B.H., et al. Disruption of dynein/dynactin inhibits axonal transport in motor neurons causing late-onset progressive degeneration. Neuron. 34:2002;715-727.
63. Zhu Q., et al. Disruption of the NF-H gene increases axonal microtubule content and velocity of neurofilament transport: relief of axonopathy resulting from the toxin β,β′-iminodipropionitrile. J. Cell Biol. 143:1998;183-193.
64. Stone J.D., et al. Neurofilaments are nonessential to the pathogenesis of toxicant-induced axonal degeneration. J. Neurosci. 21:2001;2278-2287.
65. Spittaels K., et al. Prominent axonopathy in the brain and spinal cord of transgenic mice overexpressing four-repeat human tau protein. Am. J. Pathol. 155:1999;2153-2165.
66. Lewis J., et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein. Nat. Genet. 25:2000;402-405.
67. Lewis J., et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science. 293:2001;1487-1491.
68. Stamer K., et al. Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress. J. Cell Biol. 156:2002;1051-1063.
69. Gunawardena S., Goldstein L.S. Disruption of axonal transport and neuronal viability by amyloid precursor protein mutations in Drosophila. Neuron. 32:2001;389-401.
70. Kamal A., et al. Kinesin-mediated axonal transport of a membrane compartment containing β-secretase and presenilin-1 requires APP. Nature. 414:2001;643-648.
71. Graham D.I., et al. Recent advances in neurotrauma. J. Neuropathol. Exp. Neurol. 59:2000;641-651.
72. Jafari S.S., et al. Axonal cytoskeletal changes after non-disruptive axonal injury. J. Neurocytol. 26:1997;207-221.
73. Stys P.K. Anoxic and ischemic injury of myelinated axons in CNS white matter: from mechanistic concepts to therapeutics. J. Cereb. Blood Flow Metab. 18:1998;2-25.
74. Dewar D., et al. Drug development for stroke: importance of protecting cerebral white matter. Eur. J. Pharmacol. 375:1999;41-50.