Molecular NeuroscienceExpression of the kallikrein gene family in normal and Alzheimer's disease brainShimizu-Okabe, Chigusa1,4,5; Yousef, George M.2; Diamandis, Eleftherios P.2; Yoshida, Shigetaka3; Shiosaka, Sadao4; Fahnestock, Margaret1, CAAuthor Information 1Department of Psychiatry and Behavioral Neurosciences, McMaster University, 1200 Main Street West, Hamilton, Ontario, L8N 3Z5, Canada; 2Department of Pathology and Laboratory Medicine, Mt. Sinai Hospital, Toronto, Ontario, M5G 1X5, Canada; 3Department of Anatomy 1, Asahikawa Medical College, Asahikawa 078-8510, Japan; 4Division of Structural Cell Biology, Nara Institute of Science and Technology (NAIST), Ikoma, Nara 630-0101, Japan 5Present address: Department of Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan CACorresponding Author Received 30 May 2001; accepted 27 June 2001 Neuroreport: August 28th, 2001 - Volume 12 - Issue 12 - p 2747-2751 Buy SDC Abstract The human kallikrein gene family consists of 15 serine proteases. We examined the expression of the kallikrein genes in human cerebral cortex and hippocampus by RT-PCR and compared their expression between Alzheimer's disease (AD) and control tissue. KLK1, 4, 5, 6, 7, 8, 10, 11, 13 and 14 are expressed in both cerebral cortex and hippocampus. KLK9 is expressed in cortex but not hippocampus, whereas KLK2, 3, 12 and 15 are not expressed in either tissue. We demonstrate an 11.5-fold increase in KLK8 mRNA levels in AD hippocampus compared to controls. The KLK8 gene product, neuropsin, processes extracellular matrix and is important for neuronal plasticity. Therefore, the increase in KLK8 could have detrimental effects on hippocampal function in AD. © 2001 Lippincott Williams & Wilkins, Inc.