Several epidemiological studies have shown that Alzheimer’s disease (AD) may affect twice as many women as men, although the exact reason behind this phenomenon was not yet clear. However, a recent study published in the journal Nature may provide an answer to this question.
The study, led by Professor Keqiang Ye of the Shenzhen Institute of Advanced Technology (SIAT) of the Chinese Academy of Sciences, stated that the C/EBPb/AEP pathway was the main factor driving the pathogenesis of neurodegenerative diseases.
“Based on this theory, our team discovered female hormones that change dramatically during menopause and tested which hormone selectively activates the C/EBPb/AEP pathway,” said Prof. Ye said, he said that they found follicle-stimulating hormone (FSH) to be the major pathogenic factor.
“During menopause, the serum concentration of FSH increases strongly, binding to the cognate FSH receptor on neurons and activating the C/EBPb/AEP pathway. This results in AB and tau dysregulation, leading to the development of AD. ,” said Dr. Zaidi Monae, co-corresponding author of the study and a working professor at Mount Sinai School of Medicine in New York.
What is Alzheimer’s disease:
In Alzheimer’s disease, a person gradually begins to forget everything he or she ever knew. In AD, both the patients as well as the caregivers suffer because it causes a lot of problems.
Ways to display the conclusion:
The researchers said they used ovariectomized mice to undergo anti-FSH antibody treatment, which blocked FSH and inactivated the C/EBPb/AEP pathway. Upon deletion of FSH receptor (FSHR) expression in neurons to abolish the binding of FSH to FSHR in the hippocampus, they observed that it reduced pathology and cognitive dysfunction. They also found that knockdown of C/EBPb also reduced AD pathology in the AD mice model.
They not only worked with female mice, but also injected FSH into male mice to find that it promotes AD pathology.
Test Result:
The researchers found that increased FSH after menopause binds to FSH in neurons and activates the C/EBPb/AEP pathway, which plays a key role in triggering AD pathology. They now plan to dissect the relationship between specific risk genes such as ApoE4 and FSH to find out why female ApoE4 carriers are more vulnerable to developing AD.
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