A person's risk of contracting Alzheimer's may be linked to levels of the appetite-suppressing hormone leptin, according to a US study published Wednesday which could point the way toward future treatment of the disease.
The Journal of the American Medical Association (JAMA) reported that scientists in the northeastern state of Massachusetts have found that high levels of the hormone leptin, which controls appetite, appears to be related to a reduced risk of developing Alzheimer's.
"These findings are consistent with recent experimental data indicating the leptin improves memory function in animals... and strengthens the evidence that leptin is a hormone with a broad set of actions in the central nervous system," wrote the authors of the study, researchers with the Framingham Heart Study, a 60-year-old research project under the direction of the National Heart, Lung and Blood Institute (NHLBI).
Produced by the body's fat cells, leptin sends a signal to the brain after a meal that a person has had enough to eat, thereby reducing the urge to eat.
The study measured leptin level in several hundred elderly people without dementia, with particular focus paid to a sub-group of about 200 test subjects who underwent more rigorous magnetic resonance imaging (MRI) scans.
The research, conducted over 12 years, found that subjects with the lowest levels of leptin were more likely to develop the neurological disease than those with the highest.
Twenty-five percent of test subjects with the lowest levels of leptin went on to develop Alzheimer's, according to the study, while just six percent of those with the highest leptin levels did.
The researchers said the study suggests that a patient's leptin levels eventually could be used as a marker in diagnosing the disease, or could even lead to a breakthrough in its treatment.
"If our findings our confirmed by others, leptin levels in older adults may serve as one of several possible biomarkers for healthy brain aging and, more importantly, may open new pathways for possible preventive and therapeutic intervention," the authors said.
Meanwhile another study in JAMA found that the experimental drug tarenflurbil did not appear to slow the onset or progress of Alzheimer's in patients with mild cases of the disease.
The 18-month study of 1,649 subjects found that those who took the drug did not have better outcomes in slowing cognitive decline than those given a placebo, according to the Boston University Schools of Medicine and Public Health.
An estimated 37 million people worldwide, including 5.3 million in the United States, live with dementia, with Alzheimer's disease causing the majority of cases, according to the World Health Organization (WHO).
With the aging of populations, this figure is projected to increase rapidly over the next 20 years.