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Levels of the microtubule-associated protein tau in cerebrospinal fluid (CSF-tau) were measured in samples from 87 patients with Alzheimer's disease (AD), 114 patients with non-AD neurological diseases, and 22 normal control subjects, by sandwich enzyme-linked immunosorbent assay. The CSF-tau level was significantly higher in patients with AD than in patients with non-AD neurological diseases and in controls. High CSF-tau levels were found irrespective of age at onset, apolipoprotein E genotype, clinical stage, and ethnic group. Western blots of AD CSF proteins revealed two to three immunoreactive bands with apparent molecular mass between 50 and 65 kDa, which is consistent with phosphorylated CSF-tau. These results suggest that CSF-tau reflects progressive accumulation of tau due to the progressive death of neurons in the AD brain. Assay of CSF-tau may prove to be a reliable diagnostic test for AD.

The study on the first-pass metabolism of acetaminophen was carried out in normal and thyroxine-treated rats, administered 30 mg/kg by three routes of intravenous, intraperitoneal, and oral one. Unconjugated acetaminophen and two major metabolites, glucuronide and sulfate in the plasma and urine were then measured 5 and 24 h after the administration, respectively. It was found that there was no difference in total percentage of excreted amount, independent of the routes for administration, between normal and thyroxine-treated rats. This fact shows that acetaminophen is absorbed completely from the gastrointestinal tract. However, it was also found that the extraction ratio of gastrointestinal tract in thyroxine-treated rats became smaller, and that the volume of distribution and total body clearance became larger than those in normal rats. The first-pass metabolism of acetaminophen was found to be influenced by the continuous administration of thyroxine.