Aquaporin expression in the cerebral cortex is increased at early stages of Alzheimer disease

• Published in: Brain research 2007-01, Vol.1128 (1), p.164-174
• Main Authors: Pérez, Esther, Barrachina, Marta, Rodríguez, Agustín, Torrejón-Escribano, Benjamín, Boada, Mercé, Hernández, Isabel, Sánchez, Marisa, Ferrer, Isidre
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Adult and adolescent clinical studies; Aged; Aged, 80 and over; Alzheimer disease; Alzheimer Disease - pathology; Analysis of Variance; Aquaporin 1 - metabolism; Aquaporin 4 - metabolism; Aquaporins; Biological and medical sciences; Blotting, Western - methods; Cerebral Cortex - metabolism; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Gene Expression Regulation - physiology; Humans; Immunohistochemistry - methods; Male; Medical sciences; Middle Aged; Nerve Tissue Proteins - metabolism; Neurology; Organic mental disorders. Neuropsychology; Pick disease; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Water channel
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2006.09.109

Abstract Abnormalities in the cerebral microvasculature are common in Alzheimer disease (AD). Expression levels of the water channels aquaporin 1 and aquaporin 4 (AQP1, AQP4) were examined in AD cases by gel electrophoresis and Western blotting, and densitometric values normalized with β-actin were compared with corresponding values in age-matched controls processed in parallel. In addition, samples of cases with Pick disease (PiD) were examined for comparative purposes. A significant increase in the expression levels of AQP1 was observed in AD stage II (following Braak and Braak classification). Individual variations were seen in advanced stages which resulted in non-significant differences between AD stages V–VI and age-matched controls. No differences in AQP1 levels were observed between familial AD cases (FAD, all of them at advanced stages) and corresponding age-matched controls. Immunohistochemistry showed increased AQP1 in astrocytes at early stages of AD. Double-labelling immunofluorescence and confocal microscopy disclosed AQP1 immunoreactivity at the cell surface of astrocytes which were recognized with anti-glial fibrillary acidic protein antibodies. No differences in the levels of AQP4 were observed in AD, FAD and PiD when compared with corresponding controls. These results indicate abnormal expression of AQP1 in astrocytes in AD, and they add support to the idea that abnormal regulation of mechanisms involved in the control of water fluxes occurs at early stages in AD.