How humans evolved to live longer lives
Researchers at Newcastle University have identified a collection of small adaptations in our bodies that may help to explain how humans have evolved to live longer. The study is focused on the significance of a protein called p62.
There are many cells, such as those that reside within the human brain, which need to last an entire lifetime. In order to survive, our cells have developed ways of defending themselves. A process called autophagy, for example, collects and removes damaged cell components.
“As we age, we accumulate damage in our cells and so it is thought that activating autophagy could help us treat older people suffering from dementia,” said lead author Dr. Viktor Korolchuk. “In order to be able to do this we need to understand how we can induce this cell cleaning.”
The research team managed to demonstrate how a protein called p62 is triggered to start the process of autophagy. Reactive oxygen species (ROS), which are byproducts of our metabolism that cause damage in the cell, can activate p62. The protein senses ROS and removes the damage it leaves behind, allowing the cell to survive the stress.
Although fruit flies do not naturally have p62, the researchers modified fruit flies with a human form of p62 for their study. These “humanized” flies survived longer in conditions of stress.
“This tells us that abilities like sensing stress and activating protective processes like autophagy may have evolved to allow better stress resistance and a longer lifespan,” said Dr. Korolchuk.
The study revealed that certain mutations in human p62 can prevent activation of p62 by ROS, leaving the cells unable to induce autophagy. According to the researchers, this may be the underlying cause of the premature death of neurons in patients with a neurodegenerative disease called amyotrophic lateral sclerosis (ALS).
The discovery of human adaptations like p62 help to explain how humans are living longer lives, and allows for a better understanding of how we can protect against age-related diseases.
The study is published in Nature Communications.
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