Alzheimer’s disease (AD) is an age-dependent, progressive type of dementia. It is clinically characterized by the progressive impairment of cognitive ability. Histopathologically, this disease causes the presence of amyloid plaques, neurofibrillary tangles and neuronal loss, beginning with a subtle alteration of synaptic efficacy before progressing to neuropathological changes. Importantly, the extent of synapse loss has been shown to correlate with the severity of cognitive impairment more than the degree of neuropathological changes in the AD brain.

To better understand the pathogenesis of AD, we have studied the properties of synapses in various pathophysiological conditions using both cell biological and electrophysiological methods. Recently, we have identified a synapse regulatory molecule called EphA4; it is a molecule that is involved in various neurodegenerative diseases, including AD. Currently, we have been investigating whether neuropathological changes can be cured by modulation of the EphA4 signaling pathway.