Deans' stroke musings: Tiny Fat Messengers May Link Obesity to Alzheimer’s Plaque Buildup

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, October 3, 2025

Tiny Fat Messengers May Link Obesity to Alzheimer’s Plaque Buildup

I was at exactly 25 BMI prior to stroke, then gained 35 pounds because my doctor knew nothing and did nothing to get me recovered enough to continue with all the activities that kept me in shape. 19 years later and I'm still fighting to get rid of the 'Dad' bod.

Is the waist-to-height ratio (WHtR) better at this? Mine is 38/73 inches = 0.52054 My BMI is 28.2 I think I'm pretty good. I'm overweight, but at least not obese.

Tiny Fat Messengers May Link Obesity to Alzheimer’s Plaque Buildup

Summary: A groundbreaking study reveals how obesity may drive Alzheimer’s disease through tiny messengers called extracellular vesicles released from fat tissue. These vesicles carry lipids that alter how quickly amyloid-β plaques form, a hallmark of Alzheimer’s.

Because they can cross the blood-brain barrier, they act as a direct communication line between body fat and the brain. Targeting these messengers could open new ways to prevent or slow dementia in at-risk individuals.

Key Facts:

Fat-to-Brain Link: Extracellular vesicles from body fat can cross the blood-brain barrier.
Plaque Formation: Vesicle lipids in obese individuals promote faster amyloid-β clumping.
Therapeutic Potential: Blocking this signaling may reduce Alzheimer’s risk in obesity.

Source: Houston Methodist

Obesity has long been acknowledged as a risk factor for a wide range of diseases, but a more precise link between obesity and Alzheimer’s disease has remained a mystery – until now.

A first-of-its-kind study from Houston Methodist found that adipose-derived extracellular vesicles, tiny cell-to-cell messengers in the body, can signal the buildup of amyloid-β plaque in obese individuals. These plaques are a key feature of Alzheimer’s disease.

The study, “Decoding Adipose–Brain Crosstalk: Distinct Lipid Cargo in Human Adipose-Derived Extracellular Vesicles Modulates Amyloid Aggregation in Alzheimer’s Disease,” published today in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

It explores the link between obesity, which affects about 40% of the U.S population, and the dreaded neurodegenerative disease affecting more than 7 million people in the U.S.

The research was led by Stephen Wong, Ph.D., the John S. Dunn Presidential Distinguished Chair in Biomedical Engineering . Alongside Wong, Li Yang, Ph.D., a research associate at Houston Methodist, and Jianting Sheng, Ph.D., an assistant research professor of computational biology and mathematics in radiology at the Houston Methodist Academic Institute, provided leadership in experimental design and cross-institution coordination.

“As recent studies have underscored, obesity is now recognized as the top modifiable risk factor for dementia in the United States,” said Wong, corresponding author and director of T. T. & W. F. Chao Center for BRAIN at Houston Methodist.

The researchers found that the lipid cargo of these cell messengers differs between people with obesity and lean individuals, and that the presence and levels of specific lipids that differed between the groups changed how quickly amyloid-β clumped together in laboratory models.

Using mouse models and patient body fat samples, the researchers examined the vesicles, which are tiny, membrane-bound particles that travel throughout the body and act as messengers involved in cell-to-cell communication. These minuscule communicators are also capable of crossing the blood-brain barrier.

Targeting these tiny cell messengers and disrupting their communication that leads to plaque formation may help reduce the risk of Alzheimer’s disease in people with obesity. The researchers said future work should focus on how drug therapy could stop or slow the build-up of Alzheimer’s-related toxic proteins (such as amyloid-β) in at-risk individuals.

The research was coauthored by Michael Chan, Shaohua Qi, and Bill Chan from Houston Methodist; Dharti Shantaram, Xilal Rima, Eduardo Reategui, and Willa Hsueh from The Ohio State University’s Wexner Medical Center; and Xianlin Han from the University of Texas Health Science Center at San Antonio.