In the brains of patients with DLB and PDD, most α‐synuclein aggregates are located in the presynaptic terminals and cause synaptic dysfunction via significant reduction of pre‐ and postsynaptic proteins, such as synaptophysin and drebrin.45, 46, 47 To quantitatively evaluate the effects of abnormal α‐synuclein accumulation on synaptic proteins in the frontal cortex and hippocampus, we assessed synaptophysin and synapsin I levels as presynaptic markers and drebrin and PSD‐95 levels as postsynaptic markers using capillary western blot. The gene discussed is DLG4; the disease is Lewy body dementia.