Relative attempts at modulation and manipulative processing of neurotransmitter release and
receptivity at the post-synaptic membrane appear central to the consequences of synaptic loss in
Alzheimer’s disease. In view of the ongoing dynamics of further injury to neurons in this disorder, it
would perhaps prove important to recognize consequences of disease as themselves pathogenic targets
in the evolutionary definition of further injury as progression, particularly in terms of both neuronal
cell and synapse loss.
