Journal Browser Advanced Search Help
Journal Browser Advanced search HELP
J Korean Neurol Assoc. 2008 Aug;26(3):224-230. Korean. Original Article.
Lee EH , Youn YC , Park KY , Min JH , Kwon OS , Lee HO , Hong HJ .
Department of Neurology, College of Medicine, Chung Ang University, Seoul, Korea. neudoc@cau.ac.kr
Department of Neurology, Keyo Hospital, Uiwang, Korea.
Department of Neurosurgery, Suwon woori hospital, Suwon, Korea.
Abstract

BACKGROUND: Alzheimer's disease (AD) is characterized by the pathology of amyloid plaques and tau-associated neurofibrillary tangles. Acetylcholine esterase (AChE) transforms the beta-amyloid monomer into an oligomer, and increases beta-amyloid aggregation in the brain. Increased beta-amyloid breaks the cytoskeleton of the brain by hyperphosphorylation of the tau protein. Previous studies support that AChE inhibitor has an inhibitory effect on toxicity of the beta-amyloid and phophorylated tau protein. The purpose of this study was to analyze the CSF beta-amyloid 1-42 (A beta 1-42) and phosphorylated tau protein in AD and determine their difference depending on whether AChE inhibitor was taken or not. METHODS: Subjects included 16 AD, 14 normal controls, and 15 disease controls. Nine of AD group had taken an AChE inhibitor while the remainder had not. The CSF A beta 1-42 and phosphorylated tau were measured by ELISA. RESULTS: The CSF A beta 1-42 levels were lower in AD patients than in other groups (p<0.01). We also found increased CSF A beta 1-42 levels in the AChE inhibitor users, compared with non-users. CONCLUSIONS: The level of CSF A beta 1-42 may have a diagnostic value in the patients with cognitive impairments. Also, we may expect the effect of AChE inhibitor on Alzheimer's pathology by measuring CSF A beta 1-42 levels. Therefore, the level of CSF A beta 1-42 may serve as a biological surrogate marker for AD treatment.

Copyright © 2019. Korean Association of Medical Journal Editors.