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Selective lesioning of the cholinergic neurons in the basal forebrain nuclei was a highly sought goal for use as an animal model of Alzheimer’s disease. Autopsy studies of Alzheimer’s-diseased brain tissue found that a substantial loss of the cholinergic innervation of the cerebral cortex and hippocampus was a prominent feature of this disease, and the degree of this neuron loss was highly correlated with the degree of dementia (1,2). Subsequent research confirmed that cholinergic neurons originating in the nucleus basalis of Meynert, the diagonal band of Broca, and the medial septal nucleus, which terminate mainly in the cortex, olfactory bulb, and hippocampus (3,4), are destroyed in the progression of Alzheimer’s disease. This loss occurred earlier than the degeneration of other types of neurons, and the scale of this cholinergic cell death was massive. The similarity to dopaminergic depletion in Parkinson’s disease was evident, and the cholinergic hypothesis for the dementia of Alzheimer’s disease was proposed. The need for an animal model to test therapeutic strategies fueled basic research about the function of this cholinergic basal forebrain (CBF) system.