Higher amounts of visceral abdominal fat in midlife are linked to the development of Alzheimer’s disease, according to research presented next week at the annual meeting of the Radiological Society of North America (RSNA). Visceral fat is the fat surrounding the internal organs located deep within the belly. Researchers have found that this hidden abdominal fat is linked to changes in the brain up to 15 years before the first symptoms of Alzheimer’s memory loss appear.
Increasing prevalence of Alzheimer’s disease
According to the Alzheimer’s Association, more than 6 million Americans are living with Alzheimer’s disease. By 2050, this number is expected to reach almost 13 million. One in five women and one in ten men will develop Alzheimer’s disease during their lifetime.
Identifying early risks of Alzheimer’s disease
To try to identify Alzheimer’s disease risks earlier, researchers assessed the association between brain MRI volumes, as well as amyloid and tau uptake on positron emission tomography (PET) scans. ), with body mass index (BMI), obesity, insulin strength and abdominal adipose (fat) tissue in a cognitively normal middle-aged population. Amyloid and tau are proteins thought to interfere with communication between brain cells.
Unique Study on Fat Types and Alzheimer’s Risk
“Even though other studies have linked BMI to brain atrophy or even a higher risk of dementia, no previous studies have linked a specific type of fat to the disease protein Alzheimer’s disease in cognitively normal people,” said study author Mahsa Dolatshahi, MD, MPH, a postdoctoral researcher at the Mallinckrodt Institute of Radiology (MIR) at Washington University School of Medicine in St. Louis. “Similar studies have not investigated the differential role of visceral and subcutaneous fat, particularly in terms of Alzheimer’s amyloid pathology, from midlife onwards.”
Methodology and results of the study
For this cross-sectional study, researchers analyzed data from 54 cognitively healthy participants, ages 40 to 60, with an average BMI of 32. Participants underwent glucose and insulin measurements, as well as tests glucose tolerance. The volume of subcutaneous fat (fat under the skin) and visceral fat was measured by abdominal MRI. Brain MRI measured the cortical thickness of brain regions affected by Alzheimer’s disease. PET was used to examine disease pathology in a subset of 32 participants, focusing on the amyloid plaques and tau tangles that accumulate in Alzheimer’s disease.
The researchers found that a higher visceral-to-subcutaneous fat ratio was associated with higher uptake of the amyloid tracer PET in the precuneus cortex, the region known to be affected early by amyloid pathology in Alzheimer’s disease. This relationship was worse in men than in women. Researchers also found that higher measures of visceral fat are linked to an increased burden of inflammation in the brain.
“Several pathways are suggested to play a role,” said Dr. Dolatshahi. “Inflammatory secretions of visceral fat, as opposed to the potentially protective effects of subcutaneous fat, may lead to inflammation of the brain, one of the main mechanisms contributing to Alzheimer’s disease.”
Implications for early diagnosis and intervention
Senior author Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology and director of neuromagnetic resonance imaging at MIR, noted that the findings have several key implications for diagnosis and intervention. earlier.
“This study highlights a key mechanism by which hidden fat may increase the risk of Alzheimer’s disease,” he said. “This shows that such brain changes occur on average from the age of 50, up to 15 years before the first symptoms of memory loss of Alzheimer’s disease appear.”
Dr. Raji added that the results could point to visceral fat as a therapeutic target to modify the risk of future brain inflammation and dementia.
“By going beyond body mass index by better characterizing the anatomical distribution of body fat on MRI, we now better understand why this factor can increase the risk of Alzheimer’s disease,” he said. he declares.
Other co-authors are Paul K. Commean, BEE, Joseph E. Ippolito, MD, Ph.D., Tammie LS Benzinger, MD, Ph.D., and John C. Morris, MD.
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