Dementia includes Alzheimer's disease, frontotemporal dementia, and Lewy body dementia, and the causative proteins are amyloid β (Aβ), tau, and α-synuclein, respectively.These proteins form small aggregates (oligomers) consisting of several molecules to tens of minutes in the brain, and it is said that dementia develops due to dysfunction of nerve cells. Although there are many developments of therapeutic agents that remove Aβ, their effectiveness has not been confirmed.Since many nerve cells die after the onset, prevention before the onset has recently been emphasized.

　Rifampicin is an antibiotic that has been used for many years to treat tuberculosis and leprosy, and it has been reported that leprosy patients who were taking the drug have less dementia. In 1994, Associate Professor Tomiyama confirmed the existence of the inhibitory effect of the drug on Aβ aggregation.

　This time, we investigated the action of rifampicin in vitro and discovered that it has the action of suppressing the formation of oligomers of Aβ, tau, and α-synuclein.Furthermore, in order to investigate the effect of oral administration of the drug, it was orally administered to model mice with Alzheimer's disease and frontotemporal dementia for XNUMX month.As a result, in each case, the number of oligomers in the brain decreased, synapses were restored, and improvement of memory impairment was confirmed.

　It is said that it takes more than 20 years from the aggregation of Aβ in the brain to the onset of dementia, and it is thought that taking preventive drugs will take a long time.Rifampicin is cheap and can be taken internally, and information on side effects is accumulated.In the future, if the preventive effect on humans is confirmed in clinical trials and the problem of side effects can be cleared, it is said to be promising as a safe and effective dementia preventive drug.