Abstract
It is a common premise that the irreversible loss of brain function in AD is due to the disruption of synapses and the loss of neurons that make those synapses. Accordingly, identification of the mechanisms causing circuit disruption and neuronal loss is critical to understanding and interrupting the progression of AD pathology.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Anderson, A.J., Cummings, B.J., and. Cotman, C.W., 1994, Increased immunoreactivity for Jun-and Fos-related proteins in Alzheimer’s disease: association with pathology. Exp. Neurol. 125:2286–295.
Anderson, A.J., Pike, C.J., and. Cotman, C.W., 1995, Differential induction of immediate early gene proteins in cultured neurons by beta-amyloid (Aβ): association of c-jun with Aβ-induced apoptosis. J. Neurochem. 65:1487–1498.
Beal, M.F., 1995. Aging, energy, and oxidative stress in neurodegenerative diseases. Ann. Neurol 38(3): 357–366.
Beal, M.F., Hyman, B.T., and. Koroshetz, W., 1993, Do deficits in mitochendrial energy metabolism underlie the pathology of neurodegenerative diseases? TINS 16(4): 178–184.
Behl, C., Hovey, L., Krajewski, S., Schubert, D., and. Reed, J.C., 1993, BCL-2 prevents killing of neuronal cells by glutamate but not by amyloid beta protein. Biochem. Biophys. Res. Commun. 197(2): 949–956.
Behl, M.F., 1995, Aging, energy, and oxidative stress in neurodegenerative diseases. Ann. Neurol. 38:357–366.
Butterfield, D.A., Hensley, K., Harris, M., Mattson, M., and Carney, J., 1994, â-Amyloid peptide free radical fragments initiate synaptosomal lipoperoxidation in a sequence-specific fashion: implications to Alzheimer’s disease. Biochem. Biophys. Res. Commun. 200(2):710–715.
Copani, A., Koh, J.-Y., and. Cotman, C.W, 1991, β-Amyloid increases neuronal susceptibility to injury by glucose deprivation [see comments]. NeuroReport 2(12):763–765.
Copani, A., Bruno, V., Gattalglia, G., Leanza, G., Pellitteri, R., Russo, A., Stanzani, S., and Nicholletti, F., 1995, Activation of metabotropic glutamate receptors protects cultured neurons against apoptosis induced by beta-amyloid peptide. Mol. Pharmacol. 47(5):890–897.
Cotman, C.W., and Anderson, A.J., 1995, A potential role for apoptosis in neurodegeneration and Alzheimer’s disease. Mol. Neurobiol. 10(1): 19–45.
Cotman, C.W., and Su, J.H., 1996, Mechanisms of neuronal death in Alzheimer’s disease. Brain Pathol. 67493–506.
Estus, S., Zaks, W., Freeman, R.S., Gruda M., Bravo, R., and Johnson, E.M., Jr., 1994, Altered gene expression in neurons during programmed cell death: identification of c-jun as necessary for neuronal apoptosis. J. Cell. Biol. 127(6): 1717–1727.
Finch, C.E., and. Cohen, D.M., 1997, Aging, metabolism, and Alzheimer disease: review and hypotheses. Exp. Neuro. 143(1): 82–102.
Forloni, G., Chiesa, R., Angeretti, N., and Smiroldo, S., 1993, Apoptosis mediated neurotoxicity induced by chronic application of beta amyloid fragment 25-35. Neuroreport 4(5): 523–526.
Geschwind, M., and Huber, G., 1995, Apoptotic cell death induced by beta-amyloid 1–42 peptide is cell type dependent. J. Neurochem. 65(l):292–300.
Ham, J., Babij, C., Whittleld, J., Pfarr, C.M., Lallenmand, D., Yaniv, M., and Rubin, L.L., 1995, A c-Jun dominant negative mutant protects sympathetic neurons against programmed cell death. Neuron 14(5):927–939.
Hoyer, S., 1993, Abnormalities in brain glucose utilization and its impact on cellular and molecular mechanisms in sporadic dementia of Alzheimer type. Ann. NY Acad. Sci. 695:77–80.
Loo, D.T., Copani, A.G., Pike, C.J., Whittemore, E.R., Walencewicz, A.J., and Cotman, C.W., 1993, Apoptosis is induced by beta-amyloid in cultured central nervous system neurons. Proc. Natl. Acad. Sci. USA, 90(17): 7951–7955.
Mark, R.J., Lovell, M.A., Markesbury, W.R., Uchida, K., and. Mattson, M.P., 1997, A role for 4-hydroxy-nonenal,an aldehydic product of lipid peroxidation, in disruption of ion homeostasis and neuronal death induced by amyloid beta-peptide. J. Neurochem. 68(l):255–264.
McGeer, P.L., Kamo, H., Harrop, R., Li, K.K., Tuokko, H., McGeer, E.G., Adam, M.J., Ammann, W., Beattie, B.L., and Calne, D.B., 1986, Positron emission tomography in patients with clinically diagnosed Alzheimer’s disease. Can. Med. Assoc. J. 134(6): 597–607.
Paradis, E., Douillard, H., Koutroumanis, M., Goodyer, C., and LeBlanc, A., 1996, Amyloid beta peptide of Alzheimer’s disease downregulates Bcl-2 and upregulates bax expression in human neurons. J.Neurosci. 16(23): 7533–7539.
Pike, C.J., Cummings, B.J., and Cotman, C.W., 1992, β-amyloid induces neuritic dystrophy in vitro similarities with Alzheimer pathology. Neuroreport 3:769–772.
Ratan, R.R., Murphy, T.H., and Baraban, J.M., 1994, Oxidative stress induces apoptosis in embryonic cortical neurons. J. Neurochem. 62(l):376–379.
Smith, M.A., Sayre, L.M., Monnier, V.M., and. Perry, G., 1995, Radical AGEing in Alzheimer’s disease. Trends Neurosci. 1995.18(4): 172–6.
Watt, J.A., Pike, C.J., Walencewicz-Wasserman, A.J., and Cotman, C.W., 1994, Ultrastructural analysis of β-amy-loid-induced apoptosis in cultured hippocampal neurons. Brain Res. 661:147–156.
Whittemore, E.R., Loo, D.T., and Cotman, C.W., 1994, Exposure to hydrogen peroxide induces cell death via apoptosis in cultured rat cortical neurons. NeuroReport 5(13):585–1588.
Yankner, B.A., 1996. Mechanisms of neuronal degeneration in Alzheimer’s disease. Neuron 16(5): 921–932
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1998 Springer Science+Business Media New York
About this chapter
Cite this chapter
Cotman, C.W., Pike, C.J. (1998). Apoptosis in Alzheimer’s Disease. In: Fisher, A., Hanin, I., Yoshida, M. (eds) Progress in Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 49. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5337-3_8
Download citation
DOI: https://doi.org/10.1007/978-1-4615-5337-3_8
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-7435-0
Online ISBN: 978-1-4615-5337-3
eBook Packages: Springer Book Archive