Abstract
The idea that inflammatory processes contribute to the pathology of neurodegenerative diseases and in particular of Alzheimer’s disease (AD), has been supported by epidemiological and clinical studies. Multiple retrospective epidemiological analyses indicate that patients receiving anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing AD (see McGeer and McGeer, 1995, as review). In a preliminary double-blind clinical trial, the non steroidal anti-inflammatory drug (NSAID) indomethacin has proven to reduce progression of cognitive decline in AD patients (Rogers et al., 1993). Obviously, more comprehensive clinical trials need to be carried out, but the future of anti-inflammatory therapy in AD holds great promise.
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
Amin, A. R., Vyas, P., Attur, M., Leszczynska-Piziak, J., Patel, I.R., Weissmann, G., and Abramson, S.B., 1995, The mode of action of aspirin-like drugs: effect on inducible nitric oxide synthase, Proc. Natl. A cad. Sci USA 92:7926–7930.
Curran, T., and Franza, B.R., 1988, Fos and Jim: the AP-1 connection, Cell. 55:395–397.
Gallo, V., Ciotti, M.T., Coletti, F., Aloisi, F., and Levi, G., 1982, Selective release of glutamate from rat cerebellar granule cells differentiating in culture, Proc. Natl. A cad. Sci. USA.79:7919–7923.
Garthwaite, G., and Garthwaite, J., 1989, Differential dependence on calcium of N-methyl-D-aspartate and kainate neurotoxicity in young rat hippocampal slices, Neurosci. Lett. 97:316–321.
Grilli, M., Chiu, J-S., and Lenardo, M.J., 1993, NF-KB and Rel: participants in a multiform transciptional regulatory system, Int. Rev. Cytol. 143:1–62.
Grilli, M., Ribola, M., Alberici, A., Valerio, A., Memo, M., and Spano, P.F., 1995, Identification and characterization of a kB/Rel binding site in the regulatory region of the Amyloid Precursor Protein gene, J. Biol. Chem. 270:26774–26777.
Grilli, M., Pizzi, M., Memo, M., and Spano, P.F., 1996, Neuroprotection by aspirin and sodium salicylate through blockade of NF-B activation, Science 274:1383–1385.
Grilli, M., Goffi, F., Memo, M., and Spano, P.F., 1996a, Interleukin-lβ and glutamate activate the NF-kB/Rel binding site from the regulatory region of the Amyloid Precursor Protein gene in primary neuronal cultures, J.Biol Chem. 271:15002–15007.
Guerrini, L., Blasi, F., and Denis-Donini, S., 1995, Synaptic activation of NF-êB by glutamate in cerebellar granule neurons in vitro, Proc. Natl. Acad. Sci. USA 92:9077–9081.
Insel, P., 1996, in Goodman and Gilman’s The Pharmacological Basis of Therapeutics, (McGraw-Hill, New York), pp. 617–657.
Kaltschmidt, C., Kaltschmidt, B., Neumann, H., Wekerle, H., and Baeuerle, P.A., 1994, Constitutive NFkB activity in neurons, Mol. Cell. Biol. 14:3981–3992.
Kaltschmidt, C., Kaltschmidt, B., and Baeuerle, P.A., 1995, Stimulation of ionotropic glutamate receptors activates transcription factor NF-kB in primary neurons, Proc. Natl. Acad. Sci. USA 92:9618.
Kopp, E., and Ghosh, S., 1994, Inhibition of NF-kB activity by sodium salicylate and aspirin, Science 265:956–959.
Lipton, S.A., and Rosenberg, P.A., 1995, Excitatory aminoacids as a final common pathway for neurological disorders, New Engl. J. Med. 330:613–622.
McGeer P.L., and McGeer E.G., 1995, The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases. Brain Res. Rev. 21:195–218.
Pizzi, M., Consolandi, O., Memo, M., and Spano, P.F., 1996a, Activation of multiple metabotropic glutamate receptor subtypes prevents NMDA-induced excitotoxicity in rat hippocampal slices. Eur. J. Neurosci. 8:1516–1521.
Pizzi, M., Galli, P., Consolandi, O., Arrighi, V., Memo, M., and Spano, P.F., 1996b, Metabotropic and ionotropic transducers of glutamate signal inversely control cytoplasmic Ca2+ concentration and excitotoxicity in cultured cerebellar granule cells: pivotal role of protein kinase C. Mol. Pharmacol. 49:586–594.
Rogers, J, Kirby, L.C., Hempelman, S.R., Berry, D.L., McGeer, P.L., Kaszniak, A.W., Zalinski, J., Cofield, M., Mansukhani, L., Willson, P., and Kogan, F., 1993, Clinical trial of indomethacin in Alzheimer’s disease. Neurology. 43:1609–1611.
Yan, S.D., Yan, S.F., Chen, X., Fu, J., Chen, M., Kuppusamy, P., Smith, S.M., Perry, G., Godman, G.C., Nawroth, P., Zweier, J.L., and Stern, D., 1995, Non-enzymatically glycated tau in Alzheimer’s disease induces oxidant stress resulting in cytokine gene expression and release of amyloid β-peptide. Nature Med.. 1:693–699.
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
Grilli, M. et al. (1998). Molecular Characterization of the Neuroprotective Activity of Salicylates. 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_15
Download citation
DOI: https://doi.org/10.1007/978-1-4615-5337-3_15
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-7435-0
Online ISBN: 978-1-4615-5337-3
eBook Packages: Springer Book Archive