Researchers have developed a sensor that identifies biomarkers of misfolded proteins in the blood up to 17 years before clinical symptoms appear.
As the disease progresses, disruption of protein biomarkers causes distinct deposits in the brain called plaques that aggregate between neurons and disrupt cell function.
By detecting this blood imbalance, it provides an opportunity to detect Alzheimer’s disease before any symptoms appear.
“Our aim is to determine the risk of developing Alzheimer’s dementia at a later stage with a simple blood test even before toxic plaques form in the brain, in order to ensure that treatment can be started in a timely manner,” said Professor Klaus Gerwort. , founding director of the Center for Protein Diagnostics (PRODI) at Ruhr-Universität Bochum.
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The immune infrared sensor was able to identify 68 test subjects who later developed Alzheimer’s disease with a high degree of test accuracy.
For comparison, the researchers screened for other biomarkers using the highly sensitive complementary SIMOA technology – specifically the biomarker P-tau181, which is currently proposed as a promising biomarker candidate in various studies.
“Unlike the clinical stage, this marker is not appropriate for the early, asymptomatic stage of Alzheimer’s disease,” Professor Klaus Gerwort said in a summary of the results of the comparative study.
“Surprisingly, we found that glial fiber protein (GFAP) concentration can signal disease up to 17 years before the clinical stage, although it is much less accurate than the immunological infrared sensor.”
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However, by combining the disruption of amyloid-beta formation and GFAP concentration, the researchers were able to increase the accuracy of the test in the asymptomatic phase.
The amyloid beta protein is one of the deposits that form plaques around brain cells.
The Bochum researchers hope that early diagnosis based on the disruption of amyloid-beta formation will help in applying Alzheimer’s drugs at an early stage so that they have a significantly better effect – for example, the drug Aduhelm, which was recently approved in the USA.
It is important to note that the amyloid-beta clustering theory has become mired in controversy in recent days.
A six-month investigation by Science reported “shockingly stark” evidence of tampering in a basic research paper suggesting Alzheimer’s is caused by a buildup of beta-amyloid plaques in the brain.
Commenting on the findings, Dr Sarah Imarisio, Head of Research at Alzheimer’s Research UK said: “These claims are very serious. Although we have not seen all published results that have been called into question, any allegation of scientific misconduct should be investigated and dealt with when appropriate.
“Researchers need to be able to trust the findings of their peers, so they can continue to make progress for people with conditions such as dementia.
“The amyloid protein is at the center of the most influential theory about how Alzheimer’s disease develops in the brain. But the research that has been called into question focuses on a very specific type of amyloid, and these claims do not jeopardize the vast majority of knowledge built up during decades of research about the role of this protein. in disease.”