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A fast-increasing number of data indicate that Alzheimer’s disease is a systemic disease, not restricted to the central nervous system. The nature of Alzheimer-related changes in peripheral cells confirms and emphasizes indications from biochemical and morphological studies in brain for the involvement of cellular membranes in this disease. Analysis of membrane changes in erythrocytes from Alzheimer patients suggests that the normal aging process of these cells is disturbed. These conclusions may form the basis for further studies leading to a better insight into the etiology of Alzheimer’s disease and to the development of diagnostic tools.

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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. AE-mediated chloride/bicarbonate exchange is a major component in the regulation of intracellular pH. The functional consequences of changes in AE structure may range from acidosis, disturbance of cytoskel-eton integrity, and untimely or impaired recognition of cells by components of the immune system, such as microglia. A molecular and physiological description of these changes will establish AE proteins as valuable tools in elucidating the processes of normal aging, and the disturbances in aging-related diseases such as Alzheimer’s disease.

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