Higher levels of leptin suggest brain protection against late-life dementia

Alzheimer’s disease (AD) is the leading cause of dementia. It affects an estimated 6.9 million Americans and remains the fifth-leading cause of death among Americans aged 65 and older. Unlike other major causes of death, such as HIV, heart disease, and stroke, AD rates continue to rise.

Despite its prevalence, the mechanisms behind disease development remain elusive. However, recent studies linking Alzheimer’s to midlife obesity, as well as vascular, genetic, and metabolic pathways, have the potential to reshape how the scientific community understands the neurodegenerative disease. 

Researchers from the University of Texas Health Science Center at San Antonio propose an important link between obesity and dementia in a new study. Working closely with the Framingham Heart Study — a Massachusetts-based medical research cohort dedicated to identifying common factors underlying cardiovascular disease — UT Health San Antonio scientists suggest leptin, a hormone responsible for regulating body weight, may have important implications in the pathogenesis of Alzheimer’s disease.

“Researchers from the University of Texas Health Science Center at San Antonio propose an important link between obesity and dementia in a new study.”

Leptin is a hormone responsible for the central control of food intake and metabolism. It helps regulate hunger cues and the breakdown of food. Both deficits and overproduction of leptin have been associated with obesity and uncontrollable weight fluctuations. The hormone is secreted by adipose tissue, which has been postulated to play an integral role in untangling pathways between Alzheimer’s and obesity. Leptin has been previously implicated in a variety of neurophysiological functions, including neuron development and the protection of neuronal structure and function. 

UT Health San Antonio researchers aimed to dig deeper into this relationship by conducting neuropsychological evaluations on 2,262 cognitively healthy participants from the Framingham Heart Study. The team measured concentrations of leptin and its soluble receptor through enzyme-linked assays to quantify the amount of available leptin circulating in the bloodstream. 

The results of the study indicate that higher concentrations of free leptin are associated with better white matter integrity. White matter connects different areas of the brain and nervous system through a complex set of nerve fibers, and it plays a crucial role in allowing the central nervous system to communicate with itself and respond to neural signaling. As such, weakened white matter is an important aspect of cognitive impairment caused by Alzheimer’s. Thus, findings support the putative neuroprotective role of leptin in late-life dementia risk.

Increasing leptin availability through specialized diets and lifestyle changes may hold promise in supplementing clinical Alzheimer’s treatments. While the results of this study have yet to find their place in AD medical practice, they remain part of a larger effort to redefine how medical professionals approach the neurodegenerative disease. 

Intersectional studies such as this one continue to add depth and complexity to our understanding of health and will remain a crucial part of improving diagnostic practices and viable treatment options.

“While the results of this study have yet to find their place in AD medical practice, they remain part of a larger effort to redefine how medical professionals approach the neurodegenerative disease.”