Share on PinterestObesity may speed up Alzheimer’s disease development, blood test reveals. Image credit: Olena Smyrnova/Stocksy
- Experts are interested in what factors contribute to the progression of Alzheimer’s disease.
- Recent study results suggest that obesity is linked to a faster buildup of amyloids and a faster progression of Alzheimer’s disease among individuals with obesity.
- The results suggest that addressing obesity may be another factor to address when it comes to cognitive function in the long term.
Does weight play into the risk for Alzheimer’s disease progression? Researchers from Washington University School of Medicine in St. Louis explored this question in a recent study whose results they recently presented at the annual meeting of the Radiological Society of North America (RSNA) 2025.
The results also appeared in the journal Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring in July 2025.
Based on examination of certain blood biomarkers of Alzheimer’s disease and amyloid PET scans, researchers found that people with obesity may have a faster amyloid buildup — which is linked to cognitive decline — and faster increases in Alzheimer’s disease blood biomarkers over time compared to individuals without obesity.
The research highlights the possible relationship between Alzheimer’s disease and obesity and opens the door to exploring obesity-related interventions to help address Alzheimer’s disease.
Is obesity bad for Alzheimer’s disease in the long term?
Researchers examined data from blood samples and PET scans from individuals who were part of the Alzheimer’s Disease Neuroimaging Initiative (ADNI).
In all, researchers were able to examine 1,228 plasma samples from 407 participants. The serum components they looked at were all related to Alzheimer’s disease.
Overall, there were no significant differences in how often cognitive impairment occurred in the obesity versus non-obesity group at baseline.
However, the non-obesity group actually had more individuals with high amyloid levels compared to the obesity group.
Researchers examined how blood biomarkers and amyloid levels were associated with obesity at baseline and then over time.
At baseline, obesity was actually associated with lower levels of relevant blood biomarkers and lower amyloid burden on PET scans. In this model, researchers adjusted for years of education, sex, and age.
However, the change really occurred when looking at the data in the long term. Researchers found that individuals with obesity saw faster rises in plasma levels of a protein called p-tau217 — which plays a role in Alzheimer’s disease — and the ratio of this protein, and higher long-term levels of plasma neurofilament light chain (NfL), another protein that can suggest damage to the links between neurons, called axons.
So, overall, NfL levels increased faster for the obesity group. Finally, researchers also saw a faster increase in amyloid buildup for individuals with obesity based on data from PET scans.
There was one more protein linked to Alzheimer’s that researchers examined, called plasma glial fibrillary acidic protein (GFAP), but they found that obesity did not significantly impact how much this protein level changed over time.
Study author Soheil Mohammadi, MD, a postdoctoral research associate at Mallinckrodt Institute of Radiology, Washington University in St. Louis, explained the following to Medical News Today:
“Overall, these findings indicate that while obesity is linked to a faster rate of increase in [Alzheimer’s disease]-related BBMs [blood biomarkers] and amyloid PET burden over time, this effect is not evident at baseline, likely reflecting dilution effects related to larger blood volume in individuals with obesity.”
Limitations and continued research
While valuable, this research does have certain limitations. For one thing, the limitations of the ADNI can influence this study because researchers analyzed data from this group.
Most participants had relevant observations from three timepoints, so data over even longer timeframes with more datapoints could be useful.
Researchers only corrected for certain factors in their statistical analysis, so it is possible that they did not account for relevant covariates that could have impacted the results.
Over 90% of the participants were white, which means the results cannot necessarily be generalized to other populations.
This research also focused on obesity in later life, so additional research could also explore midlife obesity.
Obesity was based on participants’ body mass index (BMI), which, while this can indicate obesity, is only an estimate and has limitations in the information it can provide. BMI can also change, and researchers only had baseline data on BMI.
Researchers note that only looking at baseline BMI might not “adequately reflect the dynamic nature of obesity.” They also note that this problem could introduce risk for reverse causation, regression to the mean, or other problems because weight loss from disease could affect results.
Certain weight loss and other problems can then make it harder to interpret biomarker levels “in the context of obesity and weight changes.”
The researchers acknowledge that certain conditions, like chronic kidney disease, could have influenced the levels of certain biomarkers. For this reason, they believe collecting data on chronic kidney disease could be helpful in future research in this area.
Finally, two authors declared conflicts of interest in the study publication. Funding of ADNI and this study is also worth considering when evaluating the study’s results, as well as the resources used, like the methods used for biomarker analysis.
The authors acknowledge that “representatives of the funding organizations contributed to the study design, data analysis and interpretation, manuscript preparation, and the decision to submit the manuscript for publication.”
Could weight management help lower dementia risk?
These findings suggest another aspect to tackle that could potentially help with slowing down the progression of Alzheimer’s disease. Obesity is a common problem experienced by many people in the United States alone.
Typically, if someone is trying to get down to a healthier weight, they can engage in more physical activity, as well as make changes to their diet.
Dung Trinh, MD, an internist at the MemorialCare Medical Group in Irvine, CA, and Chief Medical Officer of Healthy Brain Clinic, who was not involved in this study, noted the following to MNT:
“The data suggest that obesity doesn’t just correlate with Alzheimer’s — it may speed up the underlying brain changes. This opens the door to using weight management as a therapeutic strategy to slow disease progression […] If obesity increases amyloid accumulation rates, individuals with obesity might benefit from earlier screening, more frequent monitoring, or more aggressive risk-reduction interventions.”
The study results also suggest that it may be important to factor in obesity when examining certain tests and indicate the need for research into the benefits of weight management strategies.
Mohammadi noted that, “given the increasing use of BBMs [blood biomarkers] to diagnose [Alzheimer’s], our findings not only offer important context for interpreting BBM levels in individuals with versus without obesity, but also shed light on how obesity may influence [Alzheimer’s]-related pathology over time.“
“Future research could examine how weight-loss interventions affect BBM trajectories,” said the study author.
