Neural activity plays an important role in longevity

While we have long known that neural activity in the brain is responsible for disorders such as dementia and epilepsy, recent research conducted by scientists in the Blavatnik Institute at Harvard Medical School (HMS) has shown that it also plays a role in human aging and life span.

The study was published in Nature on Oct. 16. Researchers observed mice, worms, and human brains and found that a lot of activity in the brain is correlated with shorter life spans. As such, suppressing brain activity extends life spans. This is the first piece of evidence that supports the hypothesis that nervous system activity impacts longevity in humans. Past studies have demonstrated that portions of the nervous system affect animal aging, but no prior work has shown similar effects in humans.

“An intriguing aspect of our findings is that something as transient as the activity state of neural circuits could have such far-ranging consequences for physiology and life span,” said study senior author Bruce Yankner, professor of genetics at HMS and co-director of the Paul F. Glenn Center for the Biology of Aging in a HMS press release.

A chain that affects longevity, the insulin and insulin-like growth factor (IGF) signaling pathway, is apparently where neural excitation acts. An integral portion of this signaling cascade is RE1-Silencing Transcription (REST), a protein that the Yankner Lab has shown prevents brains from developing dementia and other disorders.

Neural activity is defined as all of the electrical currents and transmissions contained within the brain. Neural excitation can result in many outcomes such as a muscle twitch or a change in our mood. As for mood, the study has not yet shown if someone’s thoughts, personality, or actions change their lifespan.

“An exciting future area of research will be to determine how these findings relate to such higher-order human brain functions,” said Yankner.

Yankner and his colleagues looked at gene expression patterns in donated tissue from people who died between the ages of 60 and 100. None of these adults had dementia.

They found that those who were alive for more than 85 years expressed neural excitation genes to a lesser extent than those who died between the ages of 60 and 80. In order to test if these results were due to correlation or causation, the researchers conducted many experiments on C. elegans, genetically altered mice, and more brain tissue.

They found that blocking REST, a protein responsible for suppressing gene expression and neural activity, caused higher neural activity and earlier deaths. Centenarians’ brains contained more REST than those who died earlier.

Thanks to this study, the development of new therapies that can treat conditions involving neural excitation such as Alzheimer’s disease or bipolar disorder is imminent. In addition, the scientists have found that some forms of medicine like drugs that target REST or some actions such as meditation may be capable of increasing lifespan through the modulation of neural activity. Since human variation in neural activity may have both environmental and genetic causes, this study has opened up future avenues for therapeutic intervention.