Glycosylation of acetylcholinesterase and butyrylcholinesterase changes as a function of the duration of Alzheimer's disease

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Abstract
The identification of biochemical markers of Alzheimer's disease (AD) may help in the diagnosis of the disease. Previous studies have shown that Aβ1–42 is decreased, and tau and phospho‐tau are increased in AD cerebrospinal fluid (CSF). Our own studies have identified glycosylated isoforms of acetylcholinesterase (Glyc‐AChE) and butyrylcholinesterase (Glyc‐BuChE) that are increased in AD CSF. Glyc‐AChE is increased in APP (SW) Tg2576 transgenic mice prior to amyloid plaque deposition, which suggests that Glyc‐AChE may be an early marker of AD. The aim of this study was to determine whether Glyc‐AChE or Glyc‐BuChE is increased in CSF at early stages of AD and to compare the levels of these markers with those of Aβ1–42, tau and phospho‐tau. Lumbar CSF was obtained ante mortem from 106 non‐AD patients, including 15 patients with mild cognitive impairment (MCI), and 102 patients with probable AD. Glyc‐AChE, tau and phospho‐tau were significantly increased in the CSF of AD patients compared to non‐neurological disease (NND) controls. Aβ1–42 was lower in the AD patients than in NND controls. A positive correlation was found between the levels of Glyc‐AChE or Glyc‐BuChE and disease duration. However, there was no clear correlation between the levels of tau, phospho‐tau or Aβ1–42 and disease duration. The results suggest that Glyc‐AChE and Glyc‐BuChE are unlikely to be early markers of AD, although they may have value as markers of disease progression.
Funding Information
  • National Health and Medical Research Council of Australia
  • RL Cooper Medical Research Foundation of Australia
  • Swedish Medical Research Council
  • Axonyx Inc. (New York)
  • Innogenetics (Belgium)
  • Navarro Tripodi Foundation of Spain
  • MCyT of Spain (Ramón y Cajal Program)