The APOE4 gene, recognized as a major risk determinant for Alzheimer’s disease development, possesses the ability to subtly degrade the quality of bone structure, particularly in females. Researchers at the University of California reached this conclusion. Their findings have been documented in the journal Advanced Science (AdvSci).
While APOE4 is conventionally linked to an elevated susceptibility to neurodegenerative conditions, this novel research indicates its impact extends beyond the confines of the brain. The scientists observed that this variant also influences skeletal tissue, inducing alterations at the cellular level.
Experiments conducted on mice carrying this specific genetic configuration revealed impaired function in osteocytes—the cells responsible for maintaining bone integrity—among the female subjects. Consequently, the internal architecture of the bone tissue deteriorates, despite the bones potentially appearing typical under standard diagnostic procedures, such as density measurements.
“This suggests that bone weakening may not become apparent until a fracture occurs,” the researchers clarified.
Furthermore, the investigators identified proteins within the bone matrix that had previously been associated with Alzheimer’s disease and other brain dysfunctions. This observation may hint at a more profound biological connection between the state of the nervous system and the skeletal system than previously understood.
The authors stress that these findings currently stem from animal model testing. Nevertheless, this new body of evidence could contribute to a deeper comprehension of the concealed processes behind age-related degeneration and osteoporosis risk factors.
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