Alzheimer's disease is a degenerative neurological disease, mainly characterized by the coexistence of Aβ plaques and nerve fiber tangles in the brain, and it is essential to use samples with minimal invasiveness for early diagnosis. Particularly, platelets store and release neurotransmitters and neurotrophic factors such as serotonin and glutamate, and share many biochemical properties with neurons. In addition, it is known that abnormally activated platelets in Alzheimer's patients release Aβ and contribute to the Aβ aggregation in blood vessels. However, the role of platelets in Alzheimer's disease is not clearly defined, and studies on platelets in Alzheimer's patients are lacking. To investigate molecular mechanism in platelets, we performed platelet proteome analysis platelet proteins extracted from Alzheimer's disease (AD, n=4), amyloid-positive and negative mild cognitive impairment (MCI, n=5, n=5) and subjective memory impairment (SMI, n=4) for mass spectrometry-based profiling. As a result, a total of 4645 proteins were identified, and compared with SMI, 191 proteins were increased and 96 proteins were decreased in A+ MCI, and 39 proteins were increased and 32 proteins were decreased in AD. Among them, 6 increased proteins and 2 decreased proteins that were not differentially expressed in A-MCI were associated with Amyloid beta positivity. Therefore, we revealed potential protein biomarkers in platelets that reflect the pathogenesis of Alzheimer's disease in association with amyloid beta positivity.