K+ currents of human T-lymphocytes are unaffected by Alzheimer's disease and amyloid beta protein.
Alterations of Ca2+ homeostasis have been reported for both fibroblasts and T-lymphocytes of patients with Alzheimer's disease (AD). Considering the importance of K+ conductances for the cellular Ca2+ regulation and the recently reported absence of a K+ channel in Alzheimer fibroblasts, we investigated K+ currents in T-lymphocytes of patients with AD. In addition, the finding that amyloid beta protein affects the Ca2+ signal of T-lymphocytes and the function of K+ channels in fibroblasts prompted us to study a possible influence of amyloid beta protein fragments on K+ channels of T-lymphocytes. Our data, obtained by means of the whole-cell patch-clamp configuration on freshly isolated T-lymphocytes, indicate that K+ channels of these cells do not present any functional deficit in AD, and amyloid beta protein does not mediate an alteration of their currents.
Cohen
C D
CD
Central Institute of Mental Health, Mannheim, Germany.
Vollmayr
B
B
Aldenhoff
J B
JB
D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D004594:Electrophysiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000502:physiology; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism*; D013601:T-Lymphocytes / Q000378:metabolism*
D016229:Amyloid beta-Peptides; D015221:Potassium Channels; D002118:Calcium