Abstract
Background Acetazolamide (AZA), the only drug generally approved for hydrocephalus, is effective in only 25-30% of patients, and its effect on basal fluid flow in choroid plexus (CP) is unknown. The drug reversibly inhibits Aquaporin 4 (AQP4), the most highly expressed ‘water pore’ in the brain, and it is postulated that it reduces CSF production by modulating the expression and/or function of AQP1 (mostly found in the apical membrane of CP). In this study, we sought to elucidate the direct effect of AZA on basal fluid flow in CP.
Highlights
Acetazolamide (AZA), the only drug generally approved for hydrocephalus, is effective in only 25-30% of patients, and its effect on basal fluid flow in choroid plexus (CP) is unknown
The drug reversibly inhibits Aquaporin 4 (AQP4), the most highly expressed ‘water pore’ in the brain, and it is postulated that it reduces CSF production by modulating the expression and/or function of AQP1
The observed effect of AZA on AQP1 protein level suggests that AZA can directly modulate basal fluid flow in CP
Summary
Acetazolamide (AZA), the only drug generally approved for hydrocephalus, is effective in only 25-30% of patients, and its effect on basal fluid flow in choroid plexus (CP) is unknown. The drug reversibly inhibits Aquaporin 4 (AQP4), the most highly expressed ‘water pore’ in the brain, and it is postulated that it reduces CSF production by modulating the expression and/or function of AQP1 (mostly found in the apical membrane of CP). We sought to elucidate the direct effect of AZA on basal fluid flow in CP
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