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Memantine is a clinically well tolerated N-methyl-d-aspartate (NMDA) receptor antagonist—a review of preclinical data
TLDR
Preclinical data on memantine is summarized to provide evidence that it is indeed possible to develop clinically well tolerated NMDA receptor antagonists, a fact reflected in the recent interest of several pharmaceutical companies in developing compounds with similar properties to memantine. Expand
Glycine and N-methyl-D-aspartate receptors: physiological significance and possible therapeutic applications.
TLDR
It is shown that glycine enhances electrophysiological responses mediated by N-methyl-d-aspartate (NMDA)b-sensitive glutamatergic receptors through its role as a “spatially aggregating substance” to NMDA receptors. Expand
Modulation of l-DOPA-induced abnormal involuntary movements by clinically tested compounds: Further validation of the rat dyskinesia model
TLDR
It is indicated that axial, limb and orolingual AIMs possess predictive validity for the preclinical screening of novel antidyskinetic treatments and are suitable for selecting drugs that specifically reduce dyskinesia without diminishing the anti-akinetic effect of L-DOPA. Expand
Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system - too little activation is bad, too much is even worse
TLDR
This review summarizes existing hypotheses on the mechanism of action (MOA) of memantine in an attempt to understand how the accepted interaction with NMDA receptors could allow memantine to provide both neuroprotection and reverse deficits in learning/memory by the same MOA. Expand
Antagonism of metabotropic glutamate receptor type 5 attenuates l‐DOPA‐induced dyskinesia and its molecular and neurochemical correlates in a rat model of Parkinson’s disease
TLDR
It is demonstrated that mGluR5 antagonism produces strong anti‐dyskinetic effects in an animal model of Parkinson’s disease through central inhibition of the molecular and neurochemical underpinnings of l‐DOPA‐induced dyskinesia. Expand
Alzheimer's disease, β‐amyloid, glutamate, NMDA receptors and memantine – searching for the connections
TLDR
Strong support for the clinical relevance of such interactions is provided by the NMDA receptor antagonist memantine, which offers an excellent tool to facilitate translational extrapolations from in vitro studies through in vivo animal experiments to its ultimate clinical utility. Expand
The NMDA receptor antagonist memantine as a symptomatological and neuroprotective treatment for Alzheimer's disease: preclinical evidence
  • W. Danysz, C. Parsons
  • Psychology, Medicine
  • International journal of geriatric psychiatry
  • 1 September 2003
TLDR
It is suggested that glutamate receptors of the N‐methyl‐D‐aspartate (NMDA) type are overactivated in a tonic rather than a phasic manner in Alzheimer's disease, and memantine would be expected to improve both symptoms (cognition) and to slow down disease progression because it takes over the physiological function of magnesium. Expand
Aminoadamantanes as NMDA receptor antagonists and antiparkinsonian agents — preclinical studies
TLDR
The issue of whether NMDA antagonism plays a role in the symptomatological antiparkinsonian activity of amantadine and memantine is addressed by comparing: behaviourally effective doses, serum/brain levels, and their potency as NMDA receptor antagonists. Expand
Comparison of the potency, kinetics and voltage-dependency of a series of uncompetitive NMDA receptor antagonists in vitro with anticonvulsive and motor impairment activity in vivo
TLDR
The data from the present study do not lend support to the idea that low affinity, open channel NMDA receptor blockers are also effective in models of epilepsy at doses having little effect on physiological processes and do not contradict the known therapeutic safety of memantine and amantadine in dementia and Parkinson's disease respectively. Expand
Antidepressant-like effects of mGluR1 and mGluR5 antagonists in the rat forced swim and the mouse tail suspension tests
TLDR
It is suggested that acute blockade of mGluR5 and also of mgluR1 exerts antidepressant-like effects in behavioral despair tests in rats and mice. Expand
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