Alzheimer’s disease (AD) is a fatal disorder wherein patients suffer from sensory, motor, and cognitive loss. Currently, the identification and validation of biomarkers for diagnosing AD and other forms of dementia are increasingly important. Olfactory dysfunction is present in patients diagnosed with Alzheimer’s disease or idiopathic Parkinson's disease. Alzheimer’s patients show neuropathological changes in areas of the brain central to the olfactory processing center, suggesting the theoretical importance and potential diagnostic utility of investigating functional changes in olfaction in these patients. However, the usefulness of olfactory screens to serve as informative indicators of Alzheimer’s is precluded by the lack of knowledge regarding neural and molecular mechanisms underlying olfactory dysfunction onto Alzheimer's diseases. To test these ultimate questions, we used molecular and electrophysiological recording techniques to find out the difference of olfactory responses and AD related protein expression patterns by using fly model, Drosophila melanogaster that over-expresses the human β -amyloid, tau protein. We postulated that such flies would present with progressive olfactory impairments compared with age-matched wild type control flies. In this study, our hypothesis is that there is a correlation between olfactory deficits and the spatial expression pattern of β-amyloid and tau protein deposition. Therefore, we demonstrate a specific concentration of lesions in central olfactory structures such as antenna and Maxillary palps. Our study indicates that deficits on olfactory identification may occur in AD, which will be valuable as an indicator of neuropathogenesis.