Alzheimer’s may damage nerve connections in fat tissue

A recent study finds that Alzheimer’s disease can damage the communication between nerves and blood vessels within the body’s fat tissue. Published in the Journal of Lipid Research, this discovery suggests a mechanism by which the neurodegenerative condition may contribute to metabolic problems like heart disease and diabetes.

Alzheimer’s disease is widely recognized for its effects on memory and cognitive function. People with the condition, however, often experience a range of other health issues, including cardiovascular and metabolic disorders. A team of researchers at Houston Methodist, led by Stephen Wong, sought to understand if the disease’s impact on the body’s involuntary, or autonomic, nervous system might play a role in these associated health problems.

The body’s fat tissue, also known as adipose tissue, is a key regulator of metabolism, communicating with the brain through an intricate network of nerves and blood vessels. The team explored the possibility that Alzheimer’s interferes with these communication pathways, which could disrupt the body’s ability to properly manage its energy balance.

To investigate this connection, the researchers used a sophisticated three-dimensional imaging technique to examine fat tissue from mice. They compared tissue from a mouse model engineered to develop features of Alzheimer’s disease with tissue from healthy mice. This approach allowed them to visualize the complete structures of nerves and blood vessels as they exist within the tissue.

In the healthy mice, the images showed that sympathetic nerves, which help control metabolism, were neatly aligned with blood vessels, forming organized bundles. This close physical arrangement is considered important for efficient signaling between the nervous system and the fat cells.

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The images from the Alzheimer’s model mice showed a different arrangement. The researchers observed a “structural decoupling,” where the nerves and blood vessels had lost their close proximity to one another. The once-organized bundles were disrupted, and the signals coming from the sympathetic nerves appeared to be reduced.

This breakdown in the neurovascular structure within fat tissue could have significant consequences for a person’s health. “By disrupting the connection between the nervous system and fat tissue, the disease may impair the body’s ability to manage energy,” said Li Yang, a research associate on the study. This impairment offers a potential explanation for the heightened risk of stroke, heart disease, and diabetes seen in many people with Alzheimer’s.

Because the study was conducted in mouse models, additional work will be needed to confirm that these same changes occur in humans with the disease. The researchers suggest that their discovery points toward new possibilities for understanding and perhaps treating the condition’s broader effects.

“These insights open new avenues for research into how treating or preventing autonomic dysfunction might improve overall health outcomes for people with Alzheimer’s,” said Wong and Jianting Sheng, another key contributor to the work. Future studies could explore therapies that target this communication breakdown between the nervous system and the body’s fat tissue.

The study, “Alzheimer’s disease disrupts intra-adipose neurovascular contact,” was authored by Michelle Kwong, Jianting Sheng, Li Yang, and Stephen T. C. Wong.