Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 25, 2025 1 hour, 37 minutes ago
Medical News: A New Look at How Amyloid Beta May Harm Red Blood Cells in Alzheimer Disease
Researchers from the Institute of Biophysics and Biomedical Engineering at the Bulgarian Academy of Sciences, the Medical University Sofia in Bulgaria, and the Institute of Biophysics at the HUN-REN Biological Research Centre in Hungary have uncovered surprising new evidence that the toxic amyloid beta 42 peptide does not only damage the brain in Alzheimer disease but can also physically alter human red blood cells. These changes may weaken oxygen delivery throughout the body, especially to the brain. This
Medical News report highlights how the study helps explain why many Alzheimer patients experience worsening cognitive decline linked to reduced blood flow.
Amyloid Beta Alters Red Blood Cells in Surprising Ways
What the Study Found About Amyloid Beta in the Blood
Although amyloid beta is best known for accumulating in the brain, it also circulates in the bloodstream. The study examined how the amyloid beta 42 oligomer form—considered the most dangerous—binds to human red blood cells and changes the structure of their outer membrane. Using advanced tools such as fluorescence spectroscopy, microscopy and electrokinetic measurements, the research team showed clearly that the peptide attaches firmly to the cell surface and forms visible aggregates.
Once attached, amyloid beta caused the normally flexible membrane of red blood cells to become more rigid and tightly packed. This effect grew stronger when the cells were exposed to higher concentrations of amyloid beta or for longer periods of time. At the same time, the membrane became more electrically negative, showing clear changes in the surface charge of the cells.
How Amyloid Beta Changes Red Blood Cell Structure
The researchers discovered that healthy red blood cells have two natural membrane environments—one more fluid and one more ordered. After exposure to amyloid beta, both environments shifted toward a more ordered and less flexible state. This shift also reduced the natural diversity of the membrane regions, making the cells more uniform and more rigid overall.
Images from the study showed amyloid beta forming clusters on the red blood cell surface and even causing small spike-like protrusions to appear. These physical distortions could interfere with the cells’ ability to squeeze through small blood vessels and deliver oxygen efficiently.
Why These Findings Matter
Alzheimer disease is often viewed as a brain-only disorder, but growing evidence shows that blood flow problems may also contribute to the worsening of symptoms. The new study demonstrates that amyloid beta directly disrupts the physical properties of red blood cells, which may reduce their ability to travel smoothly through tiny vessels in the brain. Over time, this can limit oxygen supply, cause inflammation and further damage brain tissue.
The findings also suggest that red blood cells may serve as early, easy-to-access biomarkers for Alzheimer disease
, since amyloid-related changes could potentially be detected even before symptoms worsen.
Conclusion
This important research reveals that amyloid beta 42 does much more than form plaques in the brain. It can physically bind to red blood cells, stiffen their membranes, alter their electrical charge and reduce their flexibility. These changes may impair oxygen delivery to the brain and contribute to the progression of Alzheimer disease in ways that were previously underestimated. Understanding these effects opens new possibilities for early detection and new treatment strategies that target the blood as well as the brain.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/26/23/11361
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