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As the U.S. population ages and obesity rates rise, researchers are increasingly examining how these trends may intersect to drive Alzheimer’s disease (AD) risk. A review from ������Ƶ Atlantic University, published in the journal Cells, highlights growing evidence that obesity and AD are biologically connected, with fat tissue acting as an active signaling organ that influences brain health. The authors show that both conditions share early metabolic disruptions – often long before symptoms appear – suggesting risk may begin much earlier than previously understood.

The findings point to breakdowns in the body’s energy systems, particularly in mitochondria, along with inflammation and disrupted signaling from fat tissue, as key drivers of brain cell damage and cognitive decline. The review also identifies the gut-brain axis as an important factor, where imbalances in gut bacteria can further fuel inflammation and neurodegeneration. Together, the research supports a shift toward earlier detection and whole-body prevention, emphasizing that maintaining metabolic health may be critical to protecting the brain.

“Obesity and Alzheimer’s disease are closely connected through the way the body’s metabolism works,” said Shailaja Allani, Ph.D., senior author, director of the Center for Molecular Biology and Biotechnology and an associate scientist in the Department of Chemistry and Biochemistry within FAU’s Charles E. Schmidt College of Science. “Both conditions involve similar problems in how fat tissue sends signals, how the body uses insulin and how cells produce energy. Of these, problems in the mitochondria – the cell’s energy-producing structures – appear to be the most important. When mitochondria don’t work properly, it disrupts energy supply throughout the body and brain, which can contribute directly to brain cell damage and the development of Alzheimer’s disease.”

Read the press release.