TOKYO -- A team including researchers at the University of Tokyo has reported in the U.S. journal Science that experiments in mice showed that lost brain function can be restored by regulating autophagy, a cellular recycling process.

In neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), brain function, once lost, has generally been considered impossible to recover, but the finding raises hopes for technology that could reverse it.

Autophagy, the subject of the 2016 Nobel Prize in Physiology or Medicine, is a fundamental life-sustaining function that maintains cellular health by recycling cellular components. It breaks down proteins inside cells and destroys abnormal proteins. Neurodegenerative diseases occur when abnormal proteins accumulate inside nerve cells, but it had not been known whether removing those abnormal proteins could restore function.

The team developed mice in which autophagy could be selectively controlled with drugs. When the process was suppressed for four weeks, abnormal proteins accumulated inside nerve cells, and the mice showed declines in motor ability, memory and learning capacity, resembling neurodegenerative disease.

When autophagy was then restarted, abnormal proteins decreased over the next four weeks, and motor and cognitive functions recovered. The team said the findings "suggest that nerve cells may possess a greater capacity for recovery than previously thought."

Neurodegenerative diseases include not only ALS but also a wide range of disorders, such as Alzheimer's disease and other illnesses linked to abnormal proteins known as tau, as well as Parkinson's disease. Once they develop, treatment has been limited to slowing progression, with no means of restoring lost function. Some reports have also pointed to the possibility that autophagy is involved in the development of these diseases.

Noboru Mizushima, a University of Tokyo professor of cell biology on the team, said, "This could lead to treatments that restore lost function even after symptoms have appeared. We want to confirm whether recovery can also be seen in aged mice and in mice that model these diseases and then work on identifying drugs that can increase autophagy activity in humans."

(Japanese original by Ryo Watanabe, Lifestyle, Science & Environment News Department)