Pharmacological treatment of patients suffering from sporadic late-onset dementia of Alzheimer type (DAT) is controversely discussed, omitting the fact that this age-related most frequently occurring DAT form is based on a heterogenous pathogenesis, but forms a rather uniform clinical phenotype. Furthermore, sporadic late-onset DAT is influenced in two different ways, 1) by the aging process, and 2) by the disease process itself. In this context, changes in brain glucose/energy metabolism, maintenance of calcium homeostasis, and membrane stability are discussed. It is concluded that some nootropic drugs such as dihydroergotoxine, Ginkgo biloba, nicergoline, nimodipine, piracetam, and pyritinol-HCI, registered in FRG, exert a positive effect on the clinical phenotype in approximately 30% of treated cases being in an incipient state of the disease. This effect has not been proven for advanced states. There is clear evidence that Ginkgo biloba acts on membrane lability, nimodipine on the maintenance of calcium homeostasis, and both piracetam and pyritinol-HCI on glucose/energy metabolism. These diverse effects on different underlying pathogenetic abnormalities can be assumed to be the reason why only subgroups of patients respond to the treatment with nootropic drugs.