Age-Related Brain Decline Could be Reversible, Study Says

A group of neurologists at Stanford University conducted a groundbreaking study on the effects our immune cells have 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 immune system dysfunction 

The new study set out to tackle the question of what causes the immune system to grow increasingly dysfunctional as we age.

As we age, this dysfunction leads to chronic low-grade inflammation that many researchers hypothesize plays a large role in age-related diseases, such as cancer and cognitive decline.

The researchers focused on a hormone called prostaglandin E2 (PGE2), levels of which have previously been found to rise with aging. PGE2 is also known to promote inflammatory activity in immune cells.

'A double-whammy' feedback loop

Through experiments in mouse and human cells, the researchers found that PGE2 directly triggers dysfunctional inflammatory activity in macrophages, a fundamental immune white blood cell.

The scientists also demonstrated that older macrophages produce significantly more PGE2 than younger macrophages. What's more, the older counterparts also have greater surface numbers of EP2 receptors, which are responsible for binding PGE2.

This process is "a double-whammy – a positive feedback loop," Katrin Andreasson, senior author on the new study, says in a press release.

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Therapies that could 'de-age the brain'

Finally, the most compelling findings came when the researchers delved into the effects of inhibiting this PGE2-EP2 mechanism. In vitro experiments revealed that old macrophage cells transformed when the mechanism was disrupted. 

The old cells were rejuvenated when the PGE2-EP2 mechanism was inhibited and inflammatory characteristics disappeared.

The researchers then administered old mice with an experimental drug that blocks PGE2-EP2 binding. Impressively, the old mice displayed a reversal of cognitive decline and subsequently performed as well as young mice in several cognitive tests.

Andreasson suggests that such experimental drugs could eventually be used for modulating the immune system in humans and might be able to "de-age the brain."

Long research road lies ahead

Though the findings have great potential for developing a future anti-aging or anti-dementia therapy, Andreasson is quick to emphasize the fact that a long road of research and experimentation lies ahead.

She points out that the drugs used on mice in their experiments are not ready for human clinical trial yet, and they may never be safe for human consumption.

Nevertheless, the study adds to a growing field of knowledge in anti-aging science that, a few years ago, would have been confined to the realms of science-fiction.