A postbiotic could reduce the risk of damage after a traumatic brain injury, such as a concussion. Mice that had traumatic brain injuries experienced less damage and performed better on cognitive tests if they were given a postbiotic – a byproduct produced when gut bacteria digest food – before injury. This suggests the postbiotic could be given preventatively to people who are particularly at risk of traumatic brain injuries, such as military personnel.
The gut microbiome is known to influence the brain, and vice versa. Research suggests it may help modulate the effects of traumatic brain injuries, which affect tens of millions of people worldwide each year. How concussion can lead to brain damage – and what to do to prevent it The molecule indole-3-propionic acid (IPA) is produced when gut bacteria break down tryptophan, an amino acid in food such as meat, fish and eggs.
Previous studies have linked lower IPA to worse outcomes after subarachnoid haemorrhage, a rare type of stroke that causes bleeding in the brain, and in people with Alzheimer’s disease. Now, Yan Qu at the Air Force Medical University in Shaanxi, China, and his colleagues have measured it in blood samples from 106 people with traumatic brain injuries. They found that higher levels were associated with less swelling around brain lesions and better neurological outcomes six months later.
Next, the researchers – who didn’t respond to a request for an interview – induced a brain injury in mice that had been given either IPA or a control solution every day for two weeks. They found that the treated mice had less brain swelling, neuronal death and tissue damage than the control group three days later. They also performed better on tests of movement, learning and memory up to 14 days after their injury.
Traumatic brain injuries cause a series of neurological changes that occur in phases. One phase involves enzymes attacking mitochondrial membranes, causing them to disintegrate, which leads to oxidative damage. This then causes violently reactive compounds, which are usually sequestered inside mitochondria, to leak out, ultimately leading to neuroinflammation and cell death.
Through a series of imaging and cell experiments, the researchers found that IPA appeared to protect the mitochondria inside the mice’s astrocytes – cells that provide energy and support to neurons, but can become reactive and release inflammatory signals after an injury. The team traced this protective effect to IPA activating the so-called aryl hydrocarbon receptor in astrocytes, preserving their mitochondria’s function, while also suppressing immune responses linked to inflammation. But the mice were given IPA before their brain injury.
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