Neuronal anion exchange proteins in Alzheimer's disease pathology.
Anion exchange (AE) proteins are present in human neurons in the brain. Immunohistochemical data indicate that their apparent expression level increases with age, and especially with degeneration in Alzheimer's disease-affected brain areas. The increase in immunoreactivity is probably caused by changes in AE structure that lead to an increased accessibility of hitherto hidden epitopes. These epitopes correspond to regions in the membrane domain that 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 govern aging- and degeneration-associated perturbation of membrane integrity. The functional consequences of changes in AE structure may range from acidosis and disturbance of cytoskeleton integrity to untimely or impaired recognition of neurons by microglia.
Bosman
G J
GJ
Department of Biochemistry, Faculty of Medicine, University of Nijmegen, The Netherlands.
Renkawek
K
K
Van Workum
F P
FP
Bartholomeus
I G
IG
Marini
S
S
De Grip
W J
WJ
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D017920:Antiporters / Q000378:metabolism*; D001921:Brain / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D002462:Cell Membrane / Q000378:metabolism; D003599:Cytoskeleton / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007150:Immunohistochemistry; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D012016:Reference Values
D017920:Antiporters