Alzheimer’s disease is characterized by neuropathological accumulation of amyloid plaques and neurofibrillary tangles composed of amyloid-beta peptides and hyperphosphorylated tau protein, respectively. These neuropathological changes alter the function of neurons, including synaptic contacts between interacting neurons, eventually resulting in neuronal dysfunction and neurodegeneration. Here, we simultaneously isolated nerve terminals (synaptosomes) and larger sarkosyl-insoluble protein inclusions from postmortem brains from Alzheimer’s disease and control cases and performed proteomic and phosphoproteomic analyses.