Mechanisms of beta-amyloid impairment of erythrocyte function: implications for vascular alterations

It has well established that many abnormalities in vascular could be responsible for Alzheimer's Disease (AD). In particular, the reduced deformability of erythrocytes and diminished vascular NO bioavailability are two of the most suspected events associated to vascular abnormalities in AD. At this regard, it is known that NO is a regulatory factor of RBC mechanical properties, and recently we have observed that amyloid beta peptide 1-42 (Abeta) inhibits red cell nitric oxide synthase (eNOS) activity.