Abstract

Acetylcholinesterase in CSF has been observed to be post-translationally modified by abnormal glycosylation in Alzheimer’s disease. Present study was conducted to study the glycosylation profile of acetylcholinesterase (AChE) in different brain regions namely frontal and cerebral cortex and hippocampus in a rat model of dementia. The C/W ratio was calculated as percentage of AChE that did not bound to Con A (C) divided by percentage of AChE activity that did not bound to WGA (W). A retrograde dementia was induced by administering scopolamine (i.p.) 5 min prior to the first trial in passive avoidance test. No significant increase in transfer latency time on second trial after 24 h as compared to first trial indicated dementia. Tacrine, an AChE inhibitor, was studied for its effect on scopolamine dementia and AChE glycosylation pattern. C/W ratio exhibited specific alterations in the AChE glycosylation in cortex and hippocampus. In dementic rats among other brain regions there was significant increase in C/W ratio in cerebral cortex and hippocampus as compared to the control. The C/W ratio in Tacrine treated dementic rats was significantly decreased in cerebral cortex as compared to the control. Partially purified G4 and G1 molecular isoforms of AChE in rat brain revealed a differential binding pattern to lectins. The C/W ratio of G4 isoform was significantly increased in dementia as compared to control group while, G1 isoform remained unchanged. Tacrine treatment significantly increased and decreased the C/W ratio of G4 and G1 isoform, respectively as compared to the control group. Results obtained thus suggest that glycosylation of AChE was affected by alteration in learning and memory process – deficit (Scopolamine) and enhancement (Tacrine treatment).

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