In addition, and more importantly, our results reveal that NGF deprivation acts via TrkA-activation directly and locally on neurosecretory function of cholinergic presynaptic terminals by controlling the steady state levels of synapsin I, SNAP25 and α-synuclein, helping to devise rational therapies that early targets the vulnerable basalforebrain projection system in order to delay and/or reduce the onset of MCI and, ultimately, of clinical AD. The gene discussed is NGF; the disease is Alzheimer disease.