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NEUROLOGY 1993;43:1407
© 1993 American Academy of Neurology

Assessment of protein kinase C isozymes by two-site enzyme immunoassay in human brains and changes in Alzheimer's disease

S. Shimohama, MD, M. Narita, MA, H. Matsushima, MD, J. Kimura, MD, M. Kameyama, MD, M. Hagiwara, MD, H. Hidaka, MD and T. Taniguchi, PhD

Department of Neurology, Faculty of Medicine (Drs. Shimohama, Matsushima, and Kimura), Kyoto University, and the Department of Neurobiology (M. Narita and Dr. Taniguchi), Kyoto Pharmaceutical University, Kyoto; the Department of Neurology (Dr. Kameyama), Sumitomo Hospital, Osaka; and the Department of Pharmacology, Faculty of Medicine (Drs. Hagiwara and Hidaka), Nagoya University, Nagoya, Japan.

We assessed the amount of protein kinase C (PKC) in samples from postmortem normal human and Alzheimer's disease (AD) brains by a two-site enzyme immunoassay that quantitatively identified types {alpha}, ß, and {gamma} isozymes. In the normal human brain matter, type ß was the main type present, the majority of each isozyme of PKC being present in the membranous fraction of the brain tissues. In AD brains, the amount of type ß PKC was significantly reduced in the membranous fraction of the temporal cortical tissues. The amounts of types {alpha} and {gamma} in the membranous fraction and types {alpha}, ß, and {gamma} in the cytosolic fraction in AD brains were lower than in the control brains, but the difference was not significant. There was also a significant decrease in the levels of PKC in the membranous fraction of AD brains, as measured by radioactive phorbol ester binding. These results suggest that the type ß PKC isozyme is mainly present in the human temporal cortex and that reduced levels of type ß PKC in the membranous fraction may reflect a biochemical deficit related specifically to the pathogenesis of AD.

Address correspondence and reprint requests to Dr. Shun Shimohama, Department of Neurology, Faculty of Medicine, Kyoto University, 54 Shogoin Kawaharacho, Sakyo-ku, Kyoto 606, Japan.

Supported by Grants-in-Aid for Scientific Research on Priority Areas (03224105, 04268206, 04258211), a Grant-in-Aid for Encouragement of Young Scientists (04770495) from the Ministry of Education, Science and Culture, Japan, and by grants from the Sasagawa Research Foundation, the Japan Brain Foundation, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, and the Takeda Medical Research Foundation, Japan.

Received September 18,1992. Accepted for publication in final form November 3, 1992.




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[Abstract] [Full Text] [PDF]


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