Please use this identifier to cite or link to this item:
Title: Involvement of oxidative stress in the enhancement of acetylcholinesterase activity induced by amyloid beta-peptide
Authors: Melo, Joana Barbosa 
Agostinho, Paula 
Oliveira, Catarina Resende 
Keywords: Acetylcholinesterase; Beta-amyloid; Oxidative stress; Nitric oxide synthase; Retinal cells
Issue Date: 2003
Citation: Neuroscience Research. 45:1 (2003) 117-127
Abstract: Acetylcholinesterase (AChE) activity is increased within and around amyloid plaques, which are present in Alzheimer's disease (AD) patient's brain. In this study, using cultured retinal cells as a neuronal model, we analyzed the effect of the synthetic peptide A[beta]25-35 on the activity of AChE, the degradation enzyme of acetylcholine, as well as the involvement of oxidative stress in this process. The activity of AChE was increased when retinal cells were incubated with A[beta]25-35 (25 [mu]M, 24 h) and antioxidants such as [alpha]-tocopherol acetate and nitric oxide synthase (NOS) inhibitors were capable of preventing this effect. Despite A[beta]25-35 did not affect cell membrane integrity, the redox capacity of cells decreased. The incubation with this amyloidogenic peptide led to an increment of reactive oxygen species formation (20%), of lipid peroxidation (65%), and basal intracellular calcium levels (40%). The data obtained show that the enhancement of AChE activity induced by A[beta]25-35 is mediated by oxidative stress, and that vitamin E and NOS inhibitors, by preventing the compromise of the enzyme activity, can have an important role in the maintenance of acetylcholine synaptic levels, thus preventing or improving cognitive and memory functions of AD patients.
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais

Files in This Item:
File Description SizeFormat
file0477423a451149389e01d7efd8b979d7.pdf420.86 kBAdobe PDFView/Open
Show full item record

Page view(s) 50

checked on Feb 27, 2024

Download(s) 50

checked on Feb 27, 2024

Google ScholarTM


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.