Novel glycineB antagonists show neuroprotective activityin vivo

The degeneration or dysfunction of cholinergic neurons within the basal forebrain of patients with Alzheimer's disease (AD) may be related to the vulnerability of these cells to endogenous glutamate (Beal, 1995; Greenamyre and Young, 1989). The administration of drugs that attenuate the toxic a...

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Published inAmino acids Vol. 14; no. 1-3; pp. 223 - 226
Main Authors Wenk, G. L., Baker, L. M., Hauss-Wegrzyniakl, B., Danysz, W., Stoehr, J. D.
Format Journal Article
LanguageEnglish
Published Vienna Springer Nature B.V 01.03.1998
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Summary:The degeneration or dysfunction of cholinergic neurons within the basal forebrain of patients with Alzheimer's disease (AD) may be related to the vulnerability of these cells to endogenous glutamate (Beal, 1995; Greenamyre and Young, 1989). The administration of drugs that attenuate the toxic actions of glutamate in the early stages of the disease might significantly delay its rate of progression. Two approaches to neuroprotection from endogenous glutamatergic function were investigated and found to be effective: blockade of voltage-dependent, NMDA-type glutamate receptor channels and antagonism of an NMDA-receptor related glycine^sub B^ modulatory site.[PUBLICATION ABSTRACT]
ISSN:0939-4451
1438-2199
DOI:10.1007/BF01345266