Anion exchange (AE) proteins are present in human neurons in the brain. Imm
unohistochemical data indicate that their apparent expression level increas
es with age, and especially with degeneration in Alzheimer's disease-affect
ed brain areas. The increase in immunoreactivity is probably caused by chan
ges in AE structure that lead to an increased accessibility of hitherto hid
den epitopes. These epitopes correspond to regions in the membrane domain t
hat are involved in generation of senescent cell-specific antigen from AE1
in aging erythrocytes. Elucidation of the molecular nature of these changes
and the underlying mechanisms will lead to insight in the processes that g
overn aging- and degeneration-associated perturbation of membrane integrity
. The functional consequences of changes in AE structure may range from aci
dosis and disturbance of cytoskeleton integrity to untimely or impaired rec
ognition of neurons by microglia.