A study by a team of neurologists from Stanford University claims to discover the way aging makes immune cells dysfunctional that can be reversed by future anti-aging therapies.
Age and Cognitive Decline
As our bodies age, the immune system slowly fades and grows increasingly dysfunctional. For some of us, this means the immune system becomes slower in responding to infection, while for others, this means defective immune cells begin to attack healthy cells consistently.
Scientists hypothesize that chronic inflammation plays a key role in age-related diseases, especially in the brain.
According to the Center for Disease Control and Prevention, over 16 million Americans live with cognitive impairment.
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Causes of Age-Related Immune Dysfunction and Cognitive Decline
New research published in the journal Nature on Monday begun by seeking the answer to what causes age-related immune dysfunction. Whether chronic inflammatory activity played a crucial role in age-related cognitive decline and whether the cycle could be slowed or reversed.
Researchers focused on prostaglandin E2 (PGE2)-- a hormone. Previous research shows that as we age, levels of PGE2 raises and are known to promote inflammatory activities in immune cells.
The study details how PGE2 initiates inflammatory activity in fundamental white blood cells--macrophages. Animal trials and in vitro human cell testing uncovered the comprehensive chain of events that showed how PGE2 directly initiates dysfunction in macrophages.
Results confirmed that for both mouse and human cells, older macrophages produce significantly higher PGE2 compared to younger counterparts. In addition, aging macrophages present higher surface numbers of EP2 receptors that bind with PGE2.
Katrin Andreasson, senior author from the Department of Neurology and Neurological Sciences, Stanford University School of Medicine, calls the events ä double-whammy---a positive feedback loop."
The latter part of the study explores what happens when PGE2-EP2 mechanisms are inhibited. Initial experiments reveal older macrophage cells transforming when the mechanism was disrupted. In short, inflammatory characteristics disappeared, and the cells were rejuvenated.
Inhibiting the mechanism in aged mouse models resulted in more impressive results. Older mice received an experimental drug that effectively blocks PGE2-EP2 binding, displays the reversal of cognitive decline that later performs as impressively as younger mice.
Findings suggest that modulating the mechanisms in the immune system could, in theory, "de-age the brain." When PGE2-EP2 binding was isolated using a compound that couldn't cross the blood-brain barrier, cognitive improvements were still detected.
Andreasson stresses that despite the impressive results of the research, there is still a long winding path of study that must be done before a final conclusion is reached. The experimental drug that inhibits PGE2-EP2 bindings is not ready for human clinical trials.
However, the research does point to a new direction of compound development that can disrupt the dysfunctional age-related inflammatory activity.
The study suggests that cognitive aging is not an irrevocable condition. Scientists hope that the breakthrough would lead to the production of therapies that could reverse and rejuvenate the mind.
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