Günter Quack

TL;DR: 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.

TL;DR: In this paper, the authors provide an extensive review of new data related to the role of glutamate in CNS disorders, describing new aspects in glutamate and glutamatergic receptors -NMDA receptors, NR2B-selective antagonists, non-NMDA ionotropic glutamate receptors, Nacetylaspartylglutamate, and glutamate and glycine transporters.

TL;DR: 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.

TL;DR: 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.

TL;DR: It is postulate that if in Alzheimer’s disease overactivation of NMDA receptors occurs indeed, memantine would be expected to improve both symptoms (cognition) and slow down disease progression because it takes over the physiological function of magnesium.