Common fatty liver disease may cause Alzheimer’s-like symptoms

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In a new study, researchers have found the cause behind the link between non-alcoholic fatty liver disease (i.e., NAFLD, recently reclassified as metabolic associated fatty liver disease or MAFLD) and neurological problems.

The link they discovered, the unique role of an adipokine (Lipocalin-2) in causing neuroinflammation, may explain the Alzheimer’s disease-like and Parkinson’s disease-like symptoms among people with MAFLD.

These findings build on years of research conducted by the team, which has shown pathways and mechanisms between the liver and the gut microbiome with other parts of the body.

They focused on how environmental toxins contribute to liver disease, metabolic syndrome, and obesity.

The research was conducted by a team from the University of South Carolina and elsewhere.

MAFLD affects up to 25% of Americans and much of the global population—many of whom are unaware of their condition.

Yet the effects of this silent disease are far-reaching, possibly leading to cirrhosis, liver cancer/failure, and other liver diseases.

The findings from the current study not only confirm the strong correlation between MAFLD and neuroinflammation/neurodegeneration, but it explains how this happens.

The research is significant because MAFLD patients have been shown to develop Alzheimer’s and Parkinson’s-like symptoms as older adults.

Scientists can use these results to advance the knowledge in neuroinflammatory complications in MAFLD and develop appropriate treatments.

90% of the obese population and 40%—70% of those with type 2 diabetes appear to have MAFLD, according to the Centers for Disease Control and Prevention.

In addition to overweight/obese status and diabetes, other risk factors include high cholesterol and/or triglycerides, high blood pressure, and metabolic syndrome.

These people have a higher risk of having diseased livers, which are linked to increased lipocalin 2—as found in the present study.

The lipocalin 2 circulates throughout the body at higher levels, possibly inducing inflammation in the brain.

The team says chronic neuroinflammation is a critical element in the onset and progression of neurodegenerative diseases, including Alzheimer’s disease.

This study may help design a new way to counter the neuroinflammatory pathology in NASH but also in other related brain diseases associated with chronic inflammatory diseases.

One author of the study is Associate professor Saurabh Chatterjee.

The study is published in the Journal of Neuroinflammation.

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