Abstract
An immunosensor capable of high sensitivity detection of beta-amyloid peptides, shown to be a reliable biomarker for Alzheimer's disease, has been developed using screen printed graphene electrodes (SPGEs) modified with ultra-thin layers of polymerised 1,5-diaminonaphthalene (pDAN). Electropolymerization of 1,5-diaminonaphthalene (DAN) was performed to coat the graphene screen printed electrodes in a continuous polymer layer with controlled thickness. The surface characteristics of pristine graphene and polymer modified graphene electrodes were examined using Raman and X-ray photoelectron spectroscopy. The effects of polymer thickness on the electron transfer rates were investigated. An immunosensor for selective detection of beta amyloid peptides Aβ(1–42) was developed via biofunctionalization of the pDAN modified SPGE with the anti-beta amyloid antibody used as the peptide bioreceptor. The immunosensor has been used for specific detection of Aβ(1–42) with a linear range of 1 pg mL−1 to 1000 pg mL−1 and showed 1.4 pg mL−1 and 4.25 pg mL−1 detection and quantification limit, respectively. The biosensor was further validated for the analysis of spiked human plasma. The immunosensor enables rapid, accurate, precise, reproducible and highly sensitive detection of Aβ(1–42) using a low-cost SPGE platform, which opens the possibilities for diagnostic ex vivo applications and research-based real time studies.
Highlights
Alzheimer's Disease (AD) is the most common cause of dementia that in uences millions of people across the world and becomes more prevalent with aging
The polymer lms were deposited from 10 mM DAN in 0.25 M H2SO4 using standard graphene modi ed screen printed electrodes (SPGEs), where graphene was used as the working electrode, carbon as the counter electrode and Ag/AgCl as the reference electrode
Fig. S2† shows the voltammetric response of screen printed graphene electrodes (SPGEs) during the electropolymerization process
Summary
Alzheimer's Disease (AD) is the most common cause of dementia that in uences millions of people across the world and becomes more prevalent with aging. AD is a neurodegenerative disease triggered by extracellular accumulation of amyloid b peptide (Ab), intracellular appearance of neuro brillary tangles and neuronal loss.. AD is a neurodegenerative disease triggered by extracellular accumulation of amyloid b peptide (Ab), intracellular appearance of neuro brillary tangles and neuronal loss.1,2 This degeneration leads to changes in behaviour, personality and functional capacity, which deter the daily life of the patient. Gagni et al reported the detection of low CSF Ab[1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42] levels at preclinical disease stages that predicted future cognitive decline and neurodegeneration. An Ab[1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42] concentration of
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