Please view the main text area of the page by skipping the main menu.

Alzheimer's disease may be curable at very early stage: research

A team of scientists have succeeded in recovering rat brain nerve cells in a very early stage Alzheimer's-like state to an almost normal condition by removing the causal substance, it was announced on Jan. 31.

    The finding by researchers from the National Center of Neurology and Psychiatry (NCNP) and other institutions is hoped to lead to the development of treatment and preventative methods for Alzheimer's disease, whose patients number an estimated 2.5 million or more in Japan.

    While the pathogenic mechanism of Alzheimer's disease remains unknown, it is believed that the disease develops after oligomer -- an aggregation of amyloid beta protein, which is an unnecessary substance -- accumulates in the brain and leads to the gradual deaths of nerve cells. It is reportedly the first time for researchers to have demonstrated that the removal of oligomer can work to recover nerve cells from an Alzheimer's-like state.

    During the experiment, the researchers added oligomer to rat nerve cells and cultured them for two days so they develop abnormalities in proteins related to communication and other substances. They then separated those nerve cells into two groups and cultured them for another two days -- one in a solution laced with oligomer and the other in an oligomer-free solution. As a result, the researchers found that nerve cell abnormalities had further progressed in the oligomer-laced solution, while the other group had recovered to a near normal state.

    Alzheimer's disease can possibly be cured and prevented if oligomer is removed from human brain nerve cells in a very early stage of oligomer accumulation. Research has been underway worldwide for the development of drugs to prevent oligomer accumulation and for identifying the best timing for starting treatment by grasping the oligomer accumulation status.

    The latest finding was published in the British online scientific journal Molecular Brain on Jan. 31.

    Also in The Mainichi

    The Mainichi on social media

    Trending