Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 18, 2025 1 month, 2 weeks, 3 days, 18 hours, 45 minutes ago
Medical News: Fat-Derived Molecules Offer New Clues About Parkinson’s Disease
Parkinson’s disease continues to affect millions around the world, yet its underlying causes remain frustratingly unclear. Now, researchers from the Ludwik Rydygier Collegium Medicum in Bydgoszcz at Nicolaus Copernicus University in Torun are uncovering a surprising group of biological messengers that may influence how the disease develops. These messengers, known as adipokines, are substances released by body fat that unexpectedly interact with brain health, inflammation, metabolism, and even the survival of nerve cells. This
Medical News report highlights what scientists discovered about five key adipokines: leptin, adiponectin, resistin, visfatin, and progranulin.
Hidden Signals from Body Fat Drive Parkinson Disease Progression
Leptin’s Connection to Weight Loss and Nerve Damage
Leptin is usually known for controlling appetite, but research shows it also influences brain inflammation and nerve-cell survival. People with Parkinson’s often experience changes in leptin levels that match shifts in body weight, disease duration, and symptoms. Laboratory studies demonstrate that leptin can protect brain cells from toxic damage and help stabilize the mitochondria that keep neurons alive. These findings suggest leptin changes may reflect the body’s attempt to fight the disease’s growing metabolic stress.
Adiponectin’s Anti-Inflammatory Shield
Adiponectin is another adipokine with strong anti-inflammatory and antioxidant properties. In cell and animal studies, it helps protect neurons from toxins, reduces harmful oxidative stress, and supports healthier mitochondria. However, human studies show mixed results, with some Parkinson’s patients having higher adiponectin levels and others showing no difference at all. Even so, the consistent laboratory evidence highlights adiponectin’s potential as a protective biological signal.
Resistin Reveals an Unexpected Protective Side
Known mainly as a contributor to inflammation, resistin showed surprising protective effects in recent experiments. In nerve-cell models, resistin reduced oxidative stress, supported mitochondrial function, and prevented cell death caused by chemical damage. In some patients with advanced Parkinson’s symptoms, resistin levels were higher, possibly reflecting the body’s heightened inflammatory state. These findings suggest resistin could play a double role—both a sign of inflammation and a potential cellular protector, depending on the environment.
Visfatin and the Brain’s Energy Supply
Visfatin, also called NAMPT, helps cells make NAD+, a molecule essential for energy production. Researchers found that visfatin levels differ among Parkinson’s patients, especially between those with and without treatment-related complications. Because neurons rely heavily on steady NAD+ production, disturbances in visfatin may contribute to ene
rgy deficits seen in degenerating brain regions.
Progranulin’s Strong Link to Inflammation and Nerve Survival
Progranulin is one of the most promising adipokines studied so far. It helps regulate immune activity, supports lysosomal function, and prevents excessive inflammation. Lower progranulin levels were observed in many Parkinson’s patients and were closely connected to disease severity. In animal models, boosting progranulin helped protect dopamine-producing neurons from dying and reduced harmful brain inflammation. This makes progranulin a powerful candidate for future therapeutic research.
Conclusion
Adipokines—once thought to matter only for fat metabolism—are now emerging as important players in Parkinson’s disease. Their roles in inflammation, oxidative stress, mitochondrial health, and neuron protection suggest they may influence how the disease progresses. While human findings remain mixed, laboratory research shows clear biological effects. More long-term studies are needed, but adipokines may become valuable tools for early detection or even future treatment strategies aimed at slowing Parkinson’s disease.
The study findings were published in the peer reviewed journal: Molecules.
https://www.mdpi.com/1420-3049/30/22/4431
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