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A group of neurologists from Stanford University conducted a groundbreaking study on the effects of our immune cells on brain aging.
As we age, our immune cells become dysfunctional, which plays a role in many age-related diseases, New Atlas reports. However, the preliminary study suggests that this immune dysfunction may be reversible.
Exploring the dysfunction of the immune system
The new study set out to ask what causes the immune system to become more dysfunctional with age.
As we age, this dysfunction results in chronic low-grade inflammation which many researchers believe plays an important role in age-related diseases, such as cancer and cognitive decline.
The researchers focused on a hormone called prostaglandin E2 (PGE2), the levels of which increased with aging. PGE2 is also known to promote the inflammatory activity of immune cells.
A ‘double blow’ feedback loop
Through experiments on mouse and human cells, researchers found that PGE2 directly triggers dysfunctional inflammatory activity in macrophages, a fundamental immune white blood cell.
Scientists have also shown that older macrophages produce significantly more PGE2 than younger macrophages. In addition, the older homologs also have a greater surface number of EP2 receptors, which are responsible for the binding of PGE2.
This process is “a double whammy – a positive feedback loop,” says Katrin Andreasson, lead author of the new study, in a press release.
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Therapies that could ‘break the brain’
Finally, the most convincing findings came when researchers looked at the effects of inhibiting this PGE2-EP2 mechanism. In vitro experiments revealed that old macrophage cells transform when the mechanism is disrupted.
The old cells were rejuvenated when the PGE2-EP2 mechanism was inhibited and the inflammatory features disappeared.
The researchers then gave old mice an experimental drug that blocks the binding of PGE2-EP2. Impressively, the old mice showed a reversal of cognitive decline and subsequently performed as well as the young mice in several cognitive tests.
Andreasson suggests that such experimental drugs could eventually be used to modulate the immune system in humans and may be able to “degrade the brain.”
A long road of research awaits us
Although the results have great potential for developing a future anti-aging or anti-dementia therapy, Andreasson quickly insists that a long road of research and experimentation lies ahead.
She points out that the drugs used on the mice in their experiments are not yet ready for clinical trials in humans and may never be safe for human consumption.
Nonetheless, the study adds to a growing body of knowledge in anti-aging science that a few years ago would have been confined to the realms of science fiction.
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