Abstract
Alzheimer’s disease (AD) is a late-onset neurodegenerative disease characterized by progressive deterioration of cholinergic functions including learning, short-term memory, problem solving and abstract thinking. The only FDA-approved drugs for AD are potent cholinesterase inhibitors. It is well recognized, however, that cholinesterase inhibitors do not slow progress of the disease state. Our work is based on the premise that AChE plays an active role in the etiology of AD through non-catalytic neuritogenic activities of the polypeptide, and that the failure of pharmacological inhibitors of AChE to provide lasting relief is due, in part, to their activation of feedback mechanisms promoting overexpression of the protein. To study this issue, we have developed gain- and loss-of-function models of AChE gene expression.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
R. Beeri, et al., Curr. Biol. 5, 1063–71 (1995).
R. Beeri, et al., J. Neumchem 69, 2441–51 (1997).
M. Grifman and H. Soreq, Antisense and Nucleic Acid Drug Dev. 7, 351–59 (1997).
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
Seidman, S. et al. (1998). Multilevel Approaches to AChE-Induced Impairments in Learning and Memory. In: Doctor, B.P., Taylor, P., Quinn, D.M., Rotundo, R.L., Gentry, M.K. (eds) Structure and Function of Cholinesterases and Related Proteins. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1540-5_49
Download citation
DOI: https://doi.org/10.1007/978-1-4899-1540-5_49
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4899-1542-9
Online ISBN: 978-1-4899-1540-5
eBook Packages: Springer Book Archive