Obesity may quietly fast-forward Alzheimer’s disease, with blood tests revealing the change years earlier than expected.
Researchers have completed the first study to examine how obesity influences blood biomarkers linked to Alzheimer’s disease (BBMs). The findings show that these biomarkers increased as much as 95% faster in people with obesity compared with those without obesity. The research was presented at the annual meeting of the Radiological Society of North America (RSNA).
“This is the first time we’ve shown the relationship between obesity and Alzheimer’s disease as measured by blood biomarker tests,” said Cyrus Raji, M.D., Ph.D., senior author of the study and a principal investigator in the Neuroimaging Labs Research Center at Mallinckrodt Institute of Radiology (MIR) at Washington University School of Medicine in St. Louis.
Tracking Alzheimer’s Through Blood Tests and Brain Scans
The research team analyzed five years of data from 407 participants enrolled in the Alzheimer’s Disease Neuroimaging Initiative. This dataset included amyloid positron emission tomography (PET) scans along with blood samples. PET scans are used to measure amyloid burden in the brain, which reflects the buildup of beta-amyloid protein in the form of amyloid plaques, a defining feature of Alzheimer’s disease.
Blood plasma samples were examined for several BBMs associated with Alzheimer’s disease. These included pTau217 levels (a biomarker used in the diagnosis and monitoring of Alzheimer’s disease), neurofilament light chain (NfL)—a protein fragment released from damaged or dying neurons—and plasma GFAP—a protein expressed primarily in astrocytes (cells that support and protect neurons in the brain and spinal cord). All measurements were performed using six leading commercial tests.
How Body Weight Relates to Alzheimer’s Biomarkers
Researchers conducted statistical analyses to explore how BBMs were linked to body mass index (BMI), as well as how baseline obesity, time, and BBMs interacted over the study period. The blood biomarker results were also compared with amyloid PET scan findings to confirm their accuracy.
At the start of the study, higher BMI was associated with lower BBM levels and a lower overall amyloid burden across the brain. This initial result, however, did not reflect long-term disease progression.
“We believe the reduced BBMs in obese individuals was due to dilution from the higher blood volume,” said study lead author Soheil Mohammadi, M.D., M.P.H., postdoctoral research associate at MIR. “In fact, by relying on the baseline measurements, you could be fooled into thinking that the people with obesity had a lower pathology of Alzheimer’s disease. We need the longitudinal data to fully understand the how obesity impacts the development of Alzheimer’s pathology.”
A longitudinal study involves repeatedly collecting data from the same group over an extended period, tracking changes and trends over a period of time.
Faster Disease Progression Seen Over Time
As the study continued, both blood biomarkers and brain imaging revealed a different pattern. Individuals with obesity showed a greater increase in Alzheimer’s-related pathology over time compared with participants without obesity. In particular, people with obesity experienced a 29% to 95% faster rise in plasma pTau217 ratio levels. Obesity at baseline was also linked to a 24% faster increase in plasma NfL and a 3.7% faster buildup of amyloid in the brain.
Dr. Raji explained that blood-based measurements proved more sensitive than PET scans in detecting how obesity affects Alzheimer’s-related changes.
“The fact that we can track the predictive influence of obesity on rising blood biomarkers more sensitively than PET is what astonished me in this study,” he said.
Implications for Prevention and Treatment Monitoring
Dr. Mohammadi emphasized that understanding how obesity shapes amyloid accumulation and blood biomarker changes is highly relevant for clinical care and risk reduction.
“According to the 2024 report of the Lancet Commission, 14 modifiable risk factors total approximately 45%, or close to half, of the risk for Alzheimer’s disease,” he said. “If we can reduce any of those risk factors, we can significantly reduce Alzheimer’s cases or lengthen the amount of time until the onset of the disease.”
Looking ahead, Dr. Raji expects repeated blood biomarker testing combined with brain imaging to become standard practice for monitoring treatments, including anti-amyloid drugs.
“This is such profound science to follow right now because we have drugs that can treat obesity quite powerfully, which means we could track the effect of weight loss drugs on Alzheimer’s biomarkers in future studies,” he said. “It’s marvelous that we have these blood biomarkers to track the molecular pathology of Alzheimer’s disease, and MRI scans to track additional evidence of brain degeneration and response to various treatments. This work is foundational for future studies and treatment trials.”
Other co-authors are Farzaneh Rahmani, M.D., M.P.H., Mahsa Dolatshahi, M.D., M.P.H., and Suzanne E. Schindler, M.D., Ph.D.
Never miss a breakthrough: Join the SciTechDaily newsletter.
Follow us on Google and Google News.
3 Comments
With family histories of very mild food allergies and dementia I first wrote the FDA (with replies) of my early lay findings of connections between food allergies, added MSG, chronic diseases and obesity in October of 2005 (obviously, now, in-vain). Just over two decades later, researchers finding a ‘new’ connection between obesity and AD are proclaiming “This work is foundational for future studies and treatment trials.” NOT! Simply put, AD and obesity are comorbidities with obesity likely indicating a worse food allergy/MSG factor. So, yes, if you don’t eliminate the underlying causes, the more bad-diet affected victim’s AD is likely to worsen at a faster rate than the less bad-diet affected victim’s AD. Fundamental, no; useful, perhaps. Cc: two authors.
Obesity contributes to Alzheimer’s by increasing brain pressure when lying down. Obesity also causes permanent visual damage, due to increased eye pressure. The problem is that when you lie down to sleep, brain pressure and eye pressure increase due to a loss of gravity effects on circulation when lying down compared to standing up. Obesity causes worse brain pressure because the weight of the abdomen presses on the descending aorta, which shifts blood up towards the head. Head of bed elevation reduces brain pressure when lying down, and increases brain circulation, which helps reduce migraines, sleep apnea, glaucoma, strokes, and Alzheimer’s, all of which are associated with increased brain pressure. See my article, Heads Up! The Way You are Sleeping can be Killing You! https://www.academia.edu/1483361/Heads_Up_The_Way_You_Are_Sleeping_May_Be_Killing_You_
While Mr. Singer (unintentional error, prior posting) makes some good points about several effects of obesity which I can’t responsibly debate, I want to point it out again that there is a kind of very, very mild food allergy reaction (e.g., Dr. Arthur F. Coca, by 1935) that mainstream medicine still fails to recognize and research as true allergies, which can be aggravated by toxic FDA approved food additives (e.g., added MSG, approved for expanded use in 1980 with the US obesity epidemic presenting by 1994, CDC data) to cause similar harms in the absence of obesity. And, with the obesity presenting years to decades earlier than most AD, I can debate blaming obesity for what actually began as undiagnosed food allergies (medical errors) aggravated (or not) with FDA approved food poisoning and question the efficacy of treating the obesity without eliminating/mitigating the underlying causes. Ultimately, with obesity and AD being as difficult to cure as they are, effectively treating the worst symptoms, first, could be a good thing.