Original Research Article

Altered Expression of COX-2 in Subdivisions of the Hippocampus during Aging and in Alzheimer's Disease: The Hisayama Study
Kouhei Fujimi^{a, d}, Kazuhito Noda^a, Kensuke Sasaki^a, Yoshinobu Wakisaka^{a, b}, Yumihiro Tanizaki^b, Mitsuo Iida^b, Yutaka Kiyohara^c, Shigenobu Kanba^d, Toru Iwaki<sup>a

a</sup>Department of Neuropathology, Neurological Institute, Departments of
^bMedicine and Clinical Sciences,
^cEnvironmental Medicine, and
^dPsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Address of Corresponding Author

Dement Geriatr Cogn Disord 2007;23:423-431 (DOI: 10.1159/000101957)

  Key Words

• Cyclooxygenase
• Alzheimer's disease
• Hippocampus

  Abstract

Background: It has been reported that nonsteroidal anti-inflammatory drugs may delay the onset of Alzheimer's disease (AD). Since nonsteroidal anti-inflammatory drugs inhibit cyclooxygenase (COX), COX-2, an inducible form of COX, may be involved in the pathology of AD in association with the arachidonic acid cascade. In addition, it has been suggested that alterations in the balance of polyunsaturated fatty acids are associated with brain dysfunctions such as neurodegerative pathologies of the aging brain. Method: To explore COX-2 expression in the hippocampus, we analyzed 45 consecutive autopsy subjects without dementia and 25 AD patients derived from the town of Hisayama, Japan. Results: The neuronal expression of COX-2 in the CA3 subdivision of the hippocampus, subiculum, entorhinal cortex and transentorhinal cortex were consistently observed in both nondemented and AD brains, and COX-2 immunoreactivity correlated with age in nondemented brains. In AD patients, neurons of CA1 exhibited increased COX-2 immunoreactivity which correlated with the severity of AD pathology. This correlation was not apparent in nondemented subjects. Conclusion: These results suggest that COX-2 expression may be differentially regulated among subdivisions of the hippocampus and that elevated COX-2 expression in the CA1 of AD brains may be associated with AD pathology and thus cognitive dysfunction.

Copyright © 2007 S. Karger AG, Basel

  Author Contacts

Kouhei Fujimi, MD
Department of Neuropathology, Neurological Institute
Graduate School of Medical Sciences, Kyushu University
Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582 (Japan)
Tel. +81 92 642 5537, Fax +81 92 642 5540, E-Mail fujimi@np.med.kyushu-u.ac.jp

  Article Information

Accepted: March 6, 2007
Published online: April 23, 2007
Number of Print Pages : 9
Number of Figures : 6, Number of Tables : 1, Number of References : 31