Since memory loss is characteristic of Alzheimer disease (AD), and since K+ channels change during acquisition of memory in both molluscs and mammals, we investigated K+ channel function as a possible site of AD pathology and, therefore, as a possible diagnostic index as well. A 113-pS tetraethylammonium (TEA)-sensitive K+ channel was consistently absent from AD fibroblasts, while it was often present in young and aged control fibroblasts. A second (166-pS) K+ (28). Membrane potential was measured both prior to obtaining outside-out patches and by using the "perforated-patch" technique (28,37). Before recording, culture medium was replaced with the following solution (mM): NaCl 150, KCI 5, CaCl2 2, MgCl2 1, Hepes (NaOH) 10, pH = 7.4. Pipettes were made from Blue Tip capillary tubes (i.d. 1.1-1.2 mm) by using a BB-CH Mecanex puller and then filled with a high-K+ solution (mM): KCI 140, CaCl2 2, MgCl2 1, Hepes (NaOH) 10, pH = 7.4. Pipette resistances were -6 MQl. Records were obtained by using an Axopatch-1C amplifier (dc to 10 kHz), stored on tape (Toshiba PCM video recorder), and later transferred to a personal computer using an Axolab interface. Only recordings lasting for at least 3 min were considered for final analysis. The pClamp suite of programs was used for singlechannel data acquisition and analysis. Amplifier, interface, and software were obtained from Axon Instruments (Foster