Although a crucial involvement of early alterations in the NGF/TrkA system in driving neurodegeneration of basalforebrain at the onset of AD progression has been largely accepted, studies carried out on primary septohippocampal cultures have turned out to be technically challenging mainly due to the scarse yield of the cholinergic and TrkA-positive neuronal population transplanted in vitro with consequent difficulties in assessing the specificity, the precise timing and, if possible, the reversibility of any biochemical events triggered by NGF withdrawal. This evidence concerns the gene NGF and Alzheimer disease.