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Regulation of the frontocortical sodium pump by Na + in Alzheimer's disease: difference from the age‐matched control but similarity to the rat model
Author(s) -
Kairane Czeslava,
Roots Kristiina,
Uusma Tanel,
Bogdanovic Nenad,
Karelson Ello,
Kõks Sulev,
Zilmer Mihkel
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03510-x
Subject(s) - arrhenius plot , chemistry , enzyme , ibotenic acid , sodium , atpase , biophysics , medicine , endocrinology , biochemistry , biology , central nervous system , activation energy , organic chemistry
The Na + and K + dependence of the frontocortical Na,K‐ATPase in Alzheimer's disease (AD) was compared with that in human control (Co) and rat AD model. In AD, the relationship between the Na/K ratio and the Na,K‐ATPase activity showed noticeable left‐shift with three‐fold increase in the enzyme affinity for Na + ( K 0.5 =10 and 30 mM in AD and Co, respectively). The Na + dependence of the enzyme in AD showed two different Hill coefficients ( n H ), 1.1 and 0.3, whereas the Co value of n H was higher (1.4). The rat AD model generated by ibotenic acid revealed a Na + dependence similar to AD. The K + dependence of the Na,K‐ATPase showed no significant difference in AD and Co. Compared with Co, AD produced a shift in the break of the Na,K‐ATPase Arrhenius plot, suggesting remarkable alterations in the enzyme lipid environment. Our findings support the hypothesis that dysfunction of the Na,K‐ATPase in AD is provoked by altered Na + dependence of the enzyme. An impairment of the pump functionality might serve as an early mechanism of AD that should be interrupted by selective pharmacological agents.