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., Renkawek, K., Van Workum, F., Bartholomeus, I., Marini, S., De Grip, W.j. (1998). Neuronal anion exchange proteins in Alzheimer's disease pathology. In Journal of Neural Transmission, Supplement (pp.249-257). SPRINGER-VERLAG.

Neuronal anion exchange proteins in Alzheimer's disease pathology

MARINI, STEFANO;
1998-01-01

Abstract

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.
International Conference on Alzheimers Disease - From Basic Research to Clinical Applications
LEIPZIG, GERMANY
JUN 05-07, 1997
Rilevanza internazionale
1998
Settore BIO/10 - BIOCHIMICA
English
antiporter; aging; Alzheimer disease; article; cytoskeleton; immunohistochemistry; microglia; nerve degeneration; neuropathology; phagocytosis; priority journal
Intervento a convegno
Bosman, G., Renkawek, K., Van Workum, F., Bartholomeus, I., Marini, S., De Grip, W.j. (1998). Neuronal anion exchange proteins in Alzheimer's disease pathology. In Journal of Neural Transmission, Supplement (pp.249-257). SPRINGER-VERLAG.
Bosman, Gjcgm; Renkawek, K; Van Workum, Fpa; Bartholomeus, Igp; Marini, S; De Grip, Wj
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/53098
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