It’s good to always be thinking however new research shows you may want to give your brain a break sometimes.
Healthy cognition is made possible by two opposing functions: neural excitation and neural inhibition. The former makes nerves more active while the latter achieves just the opposite.
The physiological activities that regulate metabolism also play a huge role in exciting our nervous system. According to the new paper prolonged hyper-activity bears the potential to shorten our lifespan.
This hypothesis began with an examination of brain tissue extracted from deceased humans. Subjects that evidenced increased neural activity died younger than those who did not. Because the disparity was upwards of ten years, the researchers set out to identify a primary effect.
From the report: “Here we show that extended longevity in humans is associated with a distinct transcriptome signature in the cerebral cortex that is characterized by downregulation of genes related to neural excitation and synaptic function. Furthermore, longevity is dynamically regulated by the excitatory-inhibitory balance of neural circuits. ”
Engineering neural excitation and neural inhibition
Depending on the objective some species are more conducive to human translation than others. Since the researchers wanted to examine the impact neural hyperactivity has on lifespan, worm models served the criteria well, given they do not live very long.
Following several follow-up trails, the Harvard researchers were confident about excitation being a crucial correlate of longevity.
As the worms aged their brain activity naturally increased, as is the case with humans. When administered a drug that inhibited neural activity the worms lived longer than the control group. When the researchers administered a drug that stimulated neural activity the inverse was demonstrated.
This meant excitation produced a profound effect on lifespan all on its own. To locate the specific protein that was at play, the researchers swapped the worms for mice models; animals frequently employed in the service of degenerative disease research. Mice and humans share many genetic similarities. Ninety-seven percent of our working DNA is identical to be more precise.
The deceased mice analyzed showcased a neurological journey parallel to the dead worm models. Moreover, after examining the genetic material of the living rodents with a complex computer algorithm an influencing CEO protein was successfully isolated.
The expression of a protein previously linked to the progression of dementia called REST, directly surged or diminished neural activity in the mouse models.
“The transcription factor REST is upregulated in humans with extended longevity and represses excitation-related genes. Notably, REST-deficient mice exhibit increased cortical activity and neuronal excitability during aging,” the report continued. “These findings reveal a conserved mechanism of ageing that is mediated by neural circuit activity and regulated by REST.”
Though pioneering, the data is leagues away from human application. The increased and decreased REST expression was engineered for the purpose of research but there are lifestyle changes you can make to pump the brakes on neural excitation. For more on these methods please refer to an article published by Ladders on the proven benefits of interception.
“When we over-expressed or turned up, this protein in the worm, the worm now, interestingly, reduced the amount of nervous system excitation and lived longer. When we did the opposite, when we turned it down, we actually got more excitation and the worm lived a shorter lifespan,” the study’s co-author Dr. Bruce Yankner, a professor of genetics and neurology at Harvard Medical School explained to Time Magazine. “
In the same press release the professor expressed interest in furnishing the ways in which “a person’s thoughts, personality and behavior affect their overall health and longevity.”