The results for Anavex are indeed very preliminary.
The key similarity between Anavex and PBT2 is that both appear to block excitotoxicty resulting from the overactivation of NMDA receptors. This is what Namenda does as well but not particularly well. The question out there is whether a more effective inhibition of this receptor results in much highly significant improvements in cognition. At this point, we are closer to understanding the causes of Alzheimer's disease than the precise means to treat it, but once you have established a likely cause finding treatments becomes easier.
Under normal conditions of synaptic transmission, the NMDA receptor channel is blocked by Mg2+ sitting in the channel and only activated for brief periods of time. Under pathological conditions, however, overactivation of the receptor causes an excessive amount of Ca2+ influx into the nerve cell, which then triggers a variety of processes that can lead to necrosis or apoptosis. The latter processes include Ca2+ overload of mitochondria, resulting in oxygen free radical formation and activation of caspases, Ca2+-dependent activation of neuronal NOS, leading to increased NO production and the formation of toxic peroxynitrite (ONOO−), and stimulation of mitogen-activated protein kinase p38 (MAPK p38), which activates transcription factors that can go into the nucleus and influence neuronal injury and apoptosis.18,26–32
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC534915/
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