J Korean Neurol Assoc.  2008 Aug;26(3):224-230.

The Effect of Acetylcholine Esterase Inhibitor on Cerebrospinal Fluid beta-Amyloid 1-42 and Phosphorylated Tau Protein in Korean Alzheimer's Disease Patients: Preliminary Study

• Lee EH
• Youn YC
• Park KY
• Min JH
• Kwon OS
• Lee HO
• Hong HJ

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.

Keyword

Alzheimer's disease; beta-Amyloid; Tau protein; Acetylcholine esterase inhibitor

MeSH Terms

Acetylcholine
Alzheimer Disease
Biomarkers
Brain
Cytoskeleton
Humans
Neurofibrillary Tangles
Plaque, Amyloid
tau Proteins
Acetylcholine
Biological Markers
tau Proteins