Alzheimer's disease (AD) is an age-related neurodegenerative disease. AD is characterized by the presence of senile plaques, neurofibrillary tangles, and synaptic loss. Amyloid β-peptide (Aβ), a component of senile plaques, has been proposed to play an important role in oxidative stress in AD brain and could be one of the key factors in the pathogenesis of AD. In the present review, we discuss some of the AD animal models that express Aβ, and compare the proteomics-identified oxidatively modified proteins between AD brain and those of Aβ models. Such a comparison would allow better understanding of the role of Aβ in AD pathogenesis thereby helping in developing potential therapeutics to treat or delay AD.