Research has previously linked inflammation to Alzheimer’s disease (AD).
But in a recent study published in Alzheimer’s & Dementia, researchers found a surprising discovery about that link.
They found that higher levels of two chemical mediators of inflammation, known as cytokines, are linked to slower cognitive decline in older adults.
These findings could eventually be used to help identify healthy people who are at risk for the devastating neurological condition, before they have symptoms.
The study is from Massachusetts General Hospital and Harvard. One author is Rudolph Tanzi, Ph.D.
Previously, the team discovered the first AD gene linked to the immune system (or the body’s defense network that fights infection).
Since then, most new AD genes have been linked to the immune system, and many studies support the theory that immune system dysfunction plays a part in AD.
However, until now the role of the immune system in the earliest stage of AD—when brain changes characteristic of the disease silently progress in older adults without cognitive symptoms—was unclear.
In the study, the team tested 298 men and women, who were between the ages 50 and 90. All had normal cognitive abilities when they volunteered and undergo retesting annually.
The study screened each participant’s blood for nine cytokines to see if any were associated with the rate of cognitive decline and changes in the brain.
The team found that people whose brains had a big burden of amyloid beta, but who also had high levels of a pro-inflammatory cytokine called interleukin-12 (IL-12), experienced little cognitive decline.
However, men and women with elevated levels of amyloid declined more if they had a lower value of IL-12. High levels of IL-12 were also associated with fewer tau tangles.
Meanwhile, elevated levels of another pro-inflammatory cytokine, interferon-gamma (IFN-γ), were linked to slower cognitive decline, whether or not a person had deposits of amyloid.
While it may seem counterintuitive that people who were protected against cognitive decline had the highest levels of inflammation-inducing proteins in the blood, that may be an indication that their immune systems were better “primed” to fight infection, says the team.
That would fit with a theory in which the team hypothesized that amyloid-beta forms in the brain as a defense against infection, ensnaring microbial pathogens in a sticky web.
Unfortunately, the once-protective shield turns destructive over time, causing irreversible damage to neurons and synapses.
However, having high levels of IL-12 and IFN-γ may nip infections in the bud, before they can leak into the brain and induce Alzheimer’s pathology.
These results suggest that IL-12 and IFN-γ could one day be measured along with other biomarkers to predict future brain health in cognitively normal people—a tool that doesn’t yet exist in medicine.
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