A new study reveals that Alzheimer's disease may not only affect the brain, but also extend to the bone marrow, which may explain the immune system's inability to send cells to help fight the disease.
For decades, research has focused on changes occurring within the brain, particularly the accumulation of amyloid-beta protein and the formation of tau protein tangles. But the new study suggests that part of the problem may begin in the bone marrow, which produces stem cells that differentiate into various types of blood and immune cells.
The researchers focused on a type of immune cell known as "monocytes," which are cells that travel through the blood and, upon reaching tissues, can transform into phagocytic cells that help eliminate harmful substances.
Researchers found, in experiments on mice and studies involving Alzheimer's patients, that the disease affects the production of these cells within the bone marrow. It also disrupts a mechanism that is supposed to act as an alarm signal, prompting the bone marrow to send more monocytes to the brain when needed.
Experiments have shown that stem cells in the bone marrow of mice with Alzheimer's lose part of their ability to regenerate, and transform into specialized cells earlier than usual, with a defect in the production of monocytes.
The researchers also found that restoring the production of these cells in the bone marrow using targeted therapy led to an improvement in some disease manifestations in mice, and was associated with an increase in the migration of phagocytic cells to the brain.
Researchers suggest that this defect may be linked to an early depletion of the stem cells' ability to regenerate, indicating age-related changes in the circulatory system of Alzheimer's patients.
These findings add to growing evidence that Alzheimer's may not be solely a brain disease, but is also linked to changes in the immune and circulatory systems. However, the researchers emphasize that most of the experiments were conducted on mice, and further studies are needed to determine whether targeting this mechanism could lead to the development of new treatments for humans.
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