Proteins in cerebrospinal fluid can provide an early indication about the likelihood of future Alzheimer’s-related cognitive decline, according to recently published research findings out of Emory University in Atlanta.
Individuals who know they have elevated levels of these proteins could pursue “diet or lifestyle interventions,” although the research team still does not know whether the biomarkers in question are “modifiable,” Nicholas Seyfried, professor of biochemistry at Emory’s School of Medicine, said in a press release about the findings.
Seyfried, Thomas Wingo and Allan Levey — all affiliated with the Goizueta Alzheimer’s Disease Research Center at Emory — were co-senior authors of a paper recently published in Science Translational Medicine, detailing the findings of a study involving 706 participants, all of whom are taking part in the Alzheimer’s Neuroimaging Initiative. This is a long-range effort focused on detecting and tracking Alzheimer’s disease at earlier stages.
The researchers used “sensitive assay techniques” to target 48 proteins associated with Alzheimer’s disease progression, as the proteins are related to the growth of amyloid plaques and tau protein tangles, the press release stated.
“The idea is that could we come up with a peripheral marker to reflect the underlying brain pathology that’s easier to obtain, faster to run, and that we could screen population wise,” Seyfried said. “Are you higher or lower than the average? You are either in the middle, which means you’re normal, you’re below, which is probably a good thing with this protein panel. Or you’re a standard deviation above the mean. Which would indicate a risk profile.”
A second study, also coming out of the Goizueta Alzheimer’s Disease Research Center, focused on a form of Alzheimer’s that is rare, inherited and manifests in people who are 30 to 50 years old.
This research team also focused on spinal fluid proteins, comparing individuals who carry a genetic mutation and their family members who do not carry the mutation. The ratio of two proteins showed a “dramatic decline” in study participants who were nearer to the estimated year when Alzheimer’s onset would occur, while this decline was not observed in the control group without the mutation.
“We have a control group and we have a carrier group,” said first author Erik Johnson, assistant professor in Emory’s Department of Neurology and the Goizueta Alzheimer’s Disease Research Center. “If we know they’re going to develop the disease at age 50 and they’re 20 years old, we measure their spinal fluid. We know, at that point, that that measurement is estimated year of onset minus 30. And then we measure the same thing in their brother, who doesn’t carry the mutation.”
These findings were published in Nature Medicine.
“Having the ability to measure different pathways associated with a disease is really important,” said Johnson.
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