Cell Death in Nervous System Development and Neurological Disease

doi:10.1017/CBO9780511976094.011

11 - Cell Death in Nervous System Development and Neurological Disease

from Part II - Cell Death in Tissues and Organs

Published online by Cambridge University Press: 07 September 2011

Juying Li and

Edited by

Douglas R. Green: Affiliation:
St. Jude Children's Research Hospital, Memphis, Tennessee
Juying Li: Affiliation:
Harvard Medical School
Junying Yuan: Affiliation:
Harvard Medical School
John C. Reed: Affiliation:
Sanford-Burnham Medical Research Institute, La Jolla, California

Book contents

Get access

Summary

Naturally occurring neuronal cell death is common during the development of the nervous system. Depending on the neuronal population, as many as 20% to 80% of all neurons produced during embryogenesis die before the animal reaches adulthood. This regressive event functions to primarily adjust the magnitude of each neuronal population to the size or functional needs of its target field and has been recognized as a major player in establishing the definitive form of adult nervous system. Although immature neurons die physiologically in large numbers during development, mature neurons are among the most long-lived cell types in mammals. Under pathological conditions, mature neurons might activate cell death mechanisms that are known to occur in various acute and chronic neurodegenerative diseases. Pathological neuronal cell death, however, occurs through more diversified pathways than that during development. In this chapter, we review the evidence that supports the role of apoptosis during neuronal development, as well as the possible role of nonapoptotic cell death in the nervous system. We discuss the relevance of different cell death mechanisms in several neurodegenerative diseases and the potential neuroprotective targets for treatment of these diseases.

Information

Type: Chapter
Information: Apoptosis
Physiology and Pathology
, pp. 123 - 134

DOI: https://doi.org/10.1017/CBO9780511976094.011 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2011

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Book purchase

Temporarily unavailable

References

Arbour, N., Vanderluit, J. L., et al. (2008). Mcl-1 is a key regulator of apoptosis during CNS development and after DNA damage. J Neurosci 28(24): 6068–78.

Barker, P. A. (2004). p75NTR is positively promiscuous: novel partners and new insights. Neuron 42(4): 529–33.

Boillee, S., Yamanaka, K., et al. (2006). Onset and progression in inherited ALS determined by motor neurons and microglia. Science 312(5778): 1389–92.

Bonni, A., Brunet, A., et al. (1999). Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms. Science 286(5443): 1358–62.

Brunet, A., Bonni, A., et al. (1999). Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 96(6): 857–68.

Buss, R. R., Sun, W., et al. (2006). Adaptive roles of programmed cell death during nervous system development. Annu Rev Neurosci 29: 1–35.

Cardone, M. H., Roy, N., et al. (1998). Regulation of cell death protease caspase-9 by phosphorylation. Science 282(5392): 1318–21.

Carter, B. D., Kaltschmidt, C., et al. (1996). Selective activation of NF-kappa B by nerve growth factor through the neurotrophin receptor p75. Science 272(5261): 542–5.

Casaccia-Bonnefil, P., Carter, B. D., et al. (1996). Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75. Nature 383(6602): 716–9.

Cecconi, F., Alvarez-Bolado, G., et al. (1998). Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development. Cell 94(6): 727–37.

Clarke, P. G. (1981). Chance, repetition, and error in the development of normal nervous systems. Perspect Biol Med 25(1): 2–17.

Coleman, M. P. and Perry, V. H. (2002). Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurosci 25(10): 532–7.

Cowan, W. M., Fawcett, J. W., et al. (1984). Regressive events in neurogenesis. Science 225(4668): 1258–65.

Crowder, R. J. and Freeman, R. S. (1998). Phosphatidylinositol 3-kinase and Akt protein kinase are necessary and sufficient for the survival of nerve growth factor-dependent sympathetic neurons. J Neurosci 18(8): 2933–43.

Datta, S. R., Dudek, H., et al. (1997). Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell 91(2): 231–41.

Deckwerth, T. L., Elliott, J. L., et al. (1996). BAX is required for neuronal death after trophic factor deprivation and during development. Neuron 17(3): 401–11.

Gagliardini, V., Fernandez, P. A., et al. (1994). Prevention of vertebrate neuronal death by the crmA gene. Science 263(5148): 826–8.

Garcia, I., Martinou, I., et al. (1992). Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene. Science 258(5080): 302–4.

Goll, D. E., Thompson, V. F., et al. (2003). The calpain system. Physiol Rev 83(3): 731–801.

Gould, T. W., Buss, R. R., et al. (2006). Complete dissociation of motor neuron death from motor dysfunction by Bax deletion in a mouse model of ALS. J Neurosci 26(34): 8774–86.

Hengartner, M. O. and Horvitz, H. R. (1994). C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2. Cell 76(4): 665–76.

Honarpour, N., Tabuchi, K., et al. (2001). Embryonic neuronal death due to neurotrophin and neurotransmitter deprivation occurs independent of Apaf-1. Neuroscience 106(2): 263–74.

Huang, E. J. and Reichardt, L. F. (2001). Neurotrophins: roles in neuronal development and function. Annu Rev Neurosci 24: 677–736.

Huang, E. J. and Reichardt, L. F. (2003). Trk receptors: roles in neuronal signal transduction. Annu Rev Biochem 72: 609–42.

Kostic, V., Jackson-Lewis, V., et al. (1997). Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. Science 277(5325): 559–62.

Krajewska, M., Mai, J. K., et al. (2002). Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous system. Cell Death Differ 9(2): 145–57.

Kuida, K., Haydar, T. F., et al. (1998). Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Cell 94(3): 325–37.

Kuida, K., Zheng, T. S., et al. (1996). Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 384(6607): 368–72.

Lakhani, S. A., Masud, A., et al. (2006). Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311(5762): 847–51.

Lee, R., Kermani, P., et al. (2001). Regulation of cell survival by secreted proneurotrophins. Science 294(5548): 1945–8.

Levi-Montalcini, R. and Hamburger, V. (1951). Selective growth stimulating effects of mouse sarcoma on the sensory and sympathetic nervous system of the chick embryo. J Exp Zool 116(2): 321–61.

Martinou, J. C., Dubois-Dauphin, M., et al. (1994). Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia. Neuron 13(4): 1017–30.

Merry, D. E. and Korsmeyer, S. J. (1997). Bcl-2 gene family in the nervous system. Annu Rev Neurosci 20: 245–67.

Michaelidis, T. M., Sendtner, M., et al. (1996). Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development. Neuron 17(1): 75–89.

Miura, M., Zhu, H., et al. (1993). Induction of apoptosis in fibroblasts by IL-1 beta-converting enzyme, a mammalian homolog of the C. elegans cell death gene ced-3. Cell 75(4): 653–60.

Motoyama, N., Wang, F., et al. (1995). Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice. Science 267(5203): 1506–10.

Nadarajah, B. and Parnavelas, J. G. (2002). Modes of neuronal migration in the developing cerebral cortex. Nat Rev Neurosci 3(6): 423–32.

Oppenheim, R. W. (1991). Cell death during development of the nervous system. Annu Rev Neurosci 14: 453–501.

Oppenheim, R. W., Blomgren, K., et al. (2008). Developing postmitotic mammalian neurons in vivo lacking Apaf-1 undergo programmed cell death by a caspase-independent, nonapoptotic pathway involving autophagy. J Neurosci 28(6): 1490–7.

Oppenheim, R. W., Flavell, R. A., et al. (2001). Programmed cell death of developing mammalian neurons after genetic deletion of caspases. J Neurosci 21(13): 4752–60.

Raff, M. C., Whitmore, A. V., et al. (2002). Axonal self-destruction and neurodegeneration. Science 296(5569): 868–71.

Riccio, A., Ahn, S., et al. (1999). Mediation by a CREB family transcription factor of NGF-dependent survival of sympathetic neurons. Science 286(5448): 2358–61.

Snider, W. D. (1994). Functions of the neurotrophins during nervous system development: what the knockouts are teaching us. Cell 77(5): 627–38.

Sun, W., Gould, T. W., et al. (2003). Neuromuscular development after the prevention of naturally occurring neuronal death by Bax deletion. J Neurosci 23(19): 7298–310.

Terzioglu, M. and Galter, D. (2008). Parkinson's disease: genetic versus toxin-induced rodent models. FEBS J 275(7): 1384–91.

White, F. A., Keller-Peck, C. R., et al. (1998). Widespread elimination of naturally occurring neuronal death in Bax-deficient mice. J Neurosci 18(4): 1428–39.

Wishart, T. M., Parson, S. H., et al. (2006). Synaptic vulnerability in neurodegenerative disease. J Neuropathol Exp Neurol 65(8): 733–9.

Yamamoto, A., Lucas, J. J., et al. (2000). Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease. Cell 101(1): 57–66.

Yao, R. and Cooper, G. M. (1995). Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor. Science 267(5206): 2003–6.

Yuan, J., Shaham, S., et al. (1993). The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme. Cell 75(4): 641–52.

Zou, H., Henzel, W. J., et al. (1997). Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3. Cell 90(3): 405–13.

Accessibility standard: Unknown

Accessibility compliance for the PDF of this book is currently unknown and may be updated in the future.