Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss, cognitive decline, and functional disability.

AD is the most common cause of dementia and currently affects around 50 million people worldwide, and its prevalence is set to rise to 152 million by 2050. There is currently no cure for AD, and early diagnosis is essential to slow down its progression.

Researchers are constantly searching for new ways to improve the early detection of AD, and a recent study has identified a hormone called saturation hormone as a potential marker of AD risk.

What is Saturation Hormone?

Saturation hormone (SH) is a hormone produced in the gut when food is consumed. Its primary function is to signal to the brain when the body has consumed enough food, and it’s time to stop eating.

SH is known to play a role in regulating weight, glucose metabolism, and inflammation. Recent studies have suggested that SH may also be involved in cognitive function and may have a protective effect against AD.

The Study

The study, published in the Journal of Alzheimer’s Disease, analyzed data from 541 community-dwelling individuals who were followed up over 6 years.

Participants underwent extensive cognitive testing and brain imaging at baseline and follow-up visits. SH levels were measured using blood samples at the beginning of the study.

The results showed that participants with higher levels of SH at the start of the study had better cognitive function at baseline. They also had a slower rate of cognitive decline over 6 years of follow-up.

Furthermore, participants with higher levels of SH were also found to have less brain atrophy, a hallmark of AD.

Implications

The study provides evidence that SH may be a useful marker for identifying individuals at risk for AD and could be used in future diagnostic tests. The findings also suggest that increasing SH levels may have a protective effect against AD.

Further research is needed to confirm these findings and to determine how SH levels can be modified pharmacologically or through lifestyle interventions such as diet and exercise.

The Role of SH in AD

The mechanism by which SH may be involved in AD is still unclear. One possible explanation is that SH may protect against AD by reducing inflammation in the brain.

Inflammation is a key pathogenic factor in AD, and it is known to contribute to the development of amyloid plaques and tau tangles, the two hallmarks of AD. Another explanation is that SH may improve glucose metabolism, which is also known to be dysregulated in AD.

Conclusion

Further research is needed to confirm these findings and to determine how SH levels can be modified pharmacologically or through lifestyle interventions such as diet and exercise.