Selective vulnerability and pruning of phasic motoneuron axons in motoneuron disease alleviated by CNTF (original) (raw)
Coleman, P.D. & Yao, P.J. Synaptic slaughter in Alzheimer's disease. Neurobiol. Aging24, 1023–1027 (2003). ArticleCAS Google Scholar
Gurney, M.E. et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. Science264, 1772–1775 (1994). ArticleCAS Google Scholar
Bruijn, L.I., Miller, T.M. & Cleveland, D.W. Unraveling the mechanisms involved in motor neuron degeneration in ALS. Annu. Rev. Neurosci.27, 723–749 (2004). ArticleCAS Google Scholar
Frey, D. et al. Early and selective loss of neuromuscular synapse subtypes with low sprouting competence in motoneuron diseases. J. Neurosci.20, 2534–2542 (2000). ArticleCAS Google Scholar
Fischer, L.R. et al. Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man. Exp. Neurol.185, 232–240 (2004). Article Google Scholar
Lino, M.M., Schneider, C. & Caroni, P. Accumulation of SOD1 mutants in postnatal motoneurons does not cause motoneuron pathology or motoneuron disease. J. Neurosci.22, 4825–4832 (2002). ArticleCAS Google Scholar
Clement, A.M. et al. Wild-type nonneuronal cells extend survival of SOD1 mutant motor neurons in ALS mice. Science302, 113–117 (2003). ArticleCAS Google Scholar
Liu, J. et al. Toxicity of familial ALS-linked SOD1 mutants from selective recruitment to spinal mitochondria. Neuron43, 5–17 (2004). ArticleCAS Google Scholar
Pasinelli, P. et al. Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria. Neuron43, 19–30 (2004). ArticleCAS Google Scholar
Wong, P.C. et al. An adverse property of a familial ALS-linked SOD1 mutation causes motoneuron disease characterized by vacuolar degeneration of mitochondria. Neuron14, 1105–1116 (1995). ArticleCAS Google Scholar
Collard, J.F., Cote, F. & Julien, J.P. Defective axonal transport in a transgenic mouse model of amyotrophic lateral sclerosis. Nature375, 61–64 (1995). ArticleCAS Google Scholar
Zhang, B., Tu, P., Abtahian, F., Trojanowski, J.Q. & Lee, V.M. Neurofilaments and orthograde transport are reduced in ventral root axons of transgenic mice that express human SOD1 with a G93A mutation. J. Cell Biol.139, 1307–1315 (1997). ArticleCAS Google Scholar
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, 50–56 (1999). ArticleCAS Google Scholar
Pinter, M.J., Waldeck, R.F., Wallace, N. & Crok, L.C. Motor unit behavior in canine motor neuron disease. J. Neurosci.15, 3447–3457 (1995). ArticleCAS Google Scholar
Kostic, V., Jackson-Lewis, V., de Bilbao, F., Dubois-Dauphin, M. & Przedborski, S. Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. Science277, 559–562 (1997). ArticleCAS Google Scholar
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, 7727–7733 (1995). ArticleCAS Google Scholar
Lobsiger, C.S., Garcia, M.L., Ward, C.M. & Cleveland, D.W. Altered axonal architecture by removal of the heavily phosphorylated neurofilament tail domains strongly slows superoxide dismutase 1 mutant-mediated ALS. Proc. Natl. Acad. Sci. USA102, 10351–10356 (2005). ArticleCAS Google Scholar
Sagot, Y., Rosse, T., Vejsada, R., Perrelet, D. & Kato, A.C. Differential effects of neurotrophic factors on motoneuron retrograde labeling in a murine model of motoneuron disease. J. Neurosci.18, 1132–1141 (1998). ArticleCAS Google Scholar
Burke, R.E. Physiology of motor units. in Myology (eds. Engel, A.G. & Franzini-Armstrong, C.) 464–484 (McGraw-Hill, New York, 1994).
De Paola, V., Arber, S. & Caroni, P. AMPA receptors regulate dynamic equilibrium of presynaptic terminals in mature hippocampal networks. Nat. Neurosci.6, 491–500 (2003). ArticleCAS Google Scholar
Stokin, G.B. et al. Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease. Science307, 1282–1288 (2005). ArticleCAS Google Scholar
Gunawardena, S. & Goldstein, L.S. Polyglutamine diseases and transport problems: deadly traffic jams on neuronal highways. Arch. Neurol.62, 46–51 (2005). Article Google Scholar
Watts, R.J., Hoopfer, E.D. & Luo, L. Axon pruning during Drosophila metamorphosis: evidence for local degeneration and requirement of the ubiquitin-proteasome system. Neuron38, 871–885 (2003). ArticleCAS Google Scholar
Zhai, Q. et al. Involvement of the ubiquitin-proteasome system in the early stages of Wallerian degeneration. Neuron39, 217–225 (2003). ArticleCAS Google Scholar
Raff, M.C., Whitmore, A.V. & Finn, J.T. Axonal self-destruction and neurodegeneration. Science296, 868–871 (2002). ArticleCAS Google Scholar
Bruijn, L.I. et al. ALS-linked SOD1 mutant G85R mediates damage to astrocytes and promotes rapidly progressive disease with SOD1-containing inclusions. Neuron18, 327–338 (1997). ArticleCAS Google Scholar
Bommel, H. et al. Missense mutation in the tubulin-specific chaperone E (Tbce) gene in the mouse mutant progressive motor neuronopathy, a model of human motoneuron disease. J. Cell Biol.159, 563–569 (2002). ArticleCAS Google Scholar
Williamson, T.L. et al. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. Proc. Natl. Acad. Sci. USA95, 9631–9636 (1998). ArticleCAS Google Scholar
Couillard-Despres, S. et al. Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase. Proc. Natl. Acad. Sci. USA95, 9626–9630 (1998). ArticleCAS Google Scholar
Peterson, W.M., Wang, Q., Tzekova, R. & Wiegand, S.J. Ciliary neurotrophic factor and stress stimuli activate the Jak-STAT pathway in retinal neurons and glia. J. Neurosci.20, 4081–4090 (2000). ArticleCAS Google Scholar
Park, K., Luo, J.M., Hisheh, S., Harvey, A.R. & Cui, Q. Cellular mechanisms associated with spontaneous and ciliary neurotrophic factor-cAMP-induced survival and axonal regeneration of adult retinal ganglion cells. J. Neurosci.24, 10806–10815 (2004). ArticleCAS Google Scholar
Lee, H.H., Dadgostar, H., Cheng, Q., Shu, J. & Cheng, G. NF-kappaB-mediated up-regulation of Bcl-x and Bfl-1/A1 is required for CD40 survival signaling in B lymphocytes. Proc. Natl. Acad. Sci. USA96, 9136–9141 (1999). ArticleCAS Google Scholar
Delio, D.A., Fiori, M.G. & Lowndes, H.E. Motor unit function during evolution of proximal axon swellings. J. Neurol. Sci.109, 30–40 (1992). ArticleCAS Google Scholar
LaMonte, B.H. et al. Disruption of dynein/dynactin inhibits axonal transport in motor neurons causing late-onset progressive degeneration. Neuron34, 715–727 (2002). ArticleCAS Google Scholar
Xia, C.H. et al. Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A. J. Cell Biol.161, 55–66 (2003). ArticleCAS Google Scholar
Al-Chalabi, A. et al. Ciliary neurotrophic factor genotype does not influence clinical phenotype in amyotrophic lateral sclerosis. Ann. Neurol.54, 130–134 (2003). Article Google Scholar
Giess, R. et al. Early onset of severe familial amyotrophic lateral sclerosis with a SOD-1 mutation: potential impact of CNTF as a candidate modifier gene. Am. J. Hum. Genet.70, 1277–1286 (2002). ArticleCAS Google Scholar
Schaefer, A.M., Sanes, J.R. & Lichtman, J.W. A compensatory subpopulation of motor neurons in a mouse model of amyotrophic lateral sclerosis. J. Comp. Neurol.490, 209–219 (2005). Article Google Scholar
Atkin, J.D. et al. Properties of slow- and fast-twitch muscle fibres in a mouse model of amyotrophic lateral sclerosis. Neuromuscul. Disord.15, 377–388 (2005). Article Google Scholar
Raoul, C, (2002) Motoneuron death triggered by a specific pathway downstream of Fas: potentiation by ALS-linked SOD1 mutations. Neuron35, 1067–1083 (2002). ArticleCAS Google Scholar
Dengler, R. et al. Amyotrophic lateral sclerosis: macro-EMG and twitch forces of single motor units. Muscle Nerve13, 545–550 (1990). ArticleCAS Google Scholar
Larsson, L., Li, X., Tollback, A. & Grimby, L. Contractile properties in single muscle fibers from chronically overused motor units in relation to motoneuron firing properties in prior polio patients. J. Neurol. Sci.132, 182–192 (1995). ArticleCAS Google Scholar
Nguyen, M.D., Lariviere, R.C. & Julien, J.P. Reduction of axonal caliber does not alleviate motor neuron disease caused by mutant superoxide dismutase 1. Proc. Natl. Acad. Sci. USA97, 12306–12311 (2000). ArticleCAS Google Scholar
Shaw, P.J. & Eggett, C.J. Molecular factors underlying selective vulnerability of motor neurons to neurodegeneration in amyotrophic lateral sclerosis. J. Neurol.247, I17–I27 (2000). Article Google Scholar
von Lewinski, F. & Keller, B.U. Ca2+, mitochondria and selective motoneuron vulnerability: implications for ALS. Trends Neurosci.28, 494–500 (2005). ArticleCAS Google Scholar
Kuo, J.J. et al. Hyperexcitability of cultured spinal motoneurons from presymptomatic ALS mice. J. Neurophysiol.91, 571–575 (2004). Article Google Scholar
Gunawardena, S. & Goldstein, L.S. Disruption of axonal transport and neuronal viability by amyloid precursor protein mutations in Drosophila. Neuron32, 389–401 (2001). ArticleCAS Google Scholar
Gunawardena, S. et al. Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila. Neuron40, 25–40 (2003). ArticleCAS Google Scholar
Mittoux, V. et al. Restoration of cognitive and motor functions by ciliary neurotrophic factor in a primate model of Huntington's disease. Hum. Gene Ther.11, 1177–1187 (2000). ArticleCAS Google Scholar