ABSTRACT
Increasing evidence suggests that, besides the already-described deficient cholinergic transmission in AD, disturbances in glutamatergic activity may also play an important role in AD. Accumulating data suggest that NMDA receptor overactivity may contribute, via enhanced calcium ion influx, to the neuronal death that characterizes AD. On the other hand, excessive glutamate-mediated activation of receptors appears to be necessary for normal cognitive function. All in all, it is assumed that a fine equilibrium among NMDA-mediated processes should be achieved in order to maintain proper cognitive functioning. Memantine has a low to moderate affinity for the NMDA receptor, where it acts as a non-competitive antagonist that appears to block pathological , but not physiological, activation of the NMDA receptor. Memantine holds promise for the treatment of moderate to severe AD. It has been shown to improve symptoms and to reduce the rate of clinical deterioration in patients with moderate to severe AD,1 which is quite unique and does not characterize the other approved treatments for AD.
