Summary: New studies examines whether chronic liver inflammation may cause mental decline and brain inflammation as people get older. Researchers are studying how inflammatory substances released by the liver affect the brain through the study of necroptosis, a form of mobile death that causes inflammation. Early findings suggest that inhibiting liver and brain infection may contribute to maintaining mental function.
By reducing severe irritation, the study could help to develop better treatments for kidney and brain-related aging issues. Fat, a significant factor in swelling, further complicates the potential effects on heart and brain health. These findings emphasize the crucial role that liver-brain communication plays in aging-related illnesses.
Important Facts:
- Chronic kidney inflammation may cause mental decline by causing brain inflammation.
- By preventing necroptosis in the heart, inflammation in the heart and brain is lessened.
- Obesity may exacerbate infection, increasing the risk of heart and brain illnesses in aging.
Origin: University of Oklahoma
As individuals age, the heart is among many organs that experience persistent, low-grade disease, a condition that keeps the immune system activated even though there is no risk.
Although liver disease has been linked to fatty liver disease and liver cancer, the heart even communicates with the mind, causing infection that may cause mental decline. University of Oklahoma scholar Deepa Sathyaseelan, Ph. The National Institutes of Health just awarded D. a$ 2 million grant to investigate the causes of this liver-brain interaction and evaluate strategies for protecting both.
Especially, Sathyaseelan is studying necroptosis, which is a natural type of cell death with a problem: Cells that die through necroptosis burst and release elements that lead to infection. Sathyaseelan and her team made the case for the harmful effects of necroptosis in the heart as well as the decrease of those results when necroptosis was blocked in previously published research involving an aging mouse unit.
They also found that activating necroptosis in the heart increased heart disease and, unexpectedly, increased brain swelling, which affected the animal’s ability to build eggs, a possible indicator of cognitive deficits.
On the back of those studies, she received a new NIH grant to better understand how liver cell necroptosis contributes to the inflammation that both the liver and the brain experience as they get older. This understanding is necessary to ultimately develop strategies to reduce inflammation and enhance tissue function.
We hypothesized that when liver necroptosis is activated, the liver releases toxic or inflammatory molecules that cross the blood-brain barrier and cause brain inflammation there, she said.
” This kind of organ crosstalk is gaining a lot of attention in research. Usually, when we study a disease condition, we focus on one organ, but when we do that, we miss the systemic effect.
” This study tells us that, with age-associated cognitive decline or Alzheimer’s disease, we should n’t think only about targeting the brain. The role of liver inflammation also needs to be considered, according to Sathyaseelan, an assistant professor of biochemistry and physiology at the OU College of Medicine. She also works for the OU Health Stephenson Cancer Center as a researcher and for the Center for Geroscience and Healthy Brain Aging.
Sathyaseelan will investigate several additional inflammation-related factors in her study. By “eating” dead cells, macrophages are immune cells that help the body heal from infections or injuries.
However, when the body is constantly at the forefront of its own activity, macrophage behavior becomes odd and further increases inflammation.
She will also examine the role of cellular senescence in liver inflammation. Senescent cells are essentially limbo: they no longer reprogram but also do n’t pass away. Senescence can be positive if, for example, it stops the cell’s transformation into a cancer cell. But senescent cells also increase inflammation.
Sathyaseelan will investigate the impact of necroptosis on both macrophages and cellular senescence and use substances to combat inflammation that have been shown to inhibit necroptosis.
Her findings may have a wide-ranging impact on both cognitive impairment and liver disease in the aging process. Rarely are there treatments for conditions like fatty liver disease and liver cancer, and older people frequently are not candidates for liver transplants. The longer increased inflammation lasts in the brain, increasing the chance that mild cognitive impairment will develop into severe cognitive dysfunction. The prevalence of obesity, another significant cause of inflammation in the body, complicates the outlook for both conditions.
People with liver diseases have high liver inflammation and cognitive issues, according to Sabyaseelan, who said,” What we have found in our mice studies so far matches what is reported for patients.”
Our main inquiry is:” What is causing this increase in inflammation in aging?” It is crucial that we advance our knowledge in this field because it is crucial that we discover new treatments for these diseases.
Funding:
The National Institute on Aging, a division of the National Institutes of Health, supports the research presented in this news release with grant number 2R01AG059718-06A1.
The authors are solely responsible for the content of this news release, which does not necessarily reflect the National Institutes of Health’s official positions. This study was also financially supported by the Presbyterian Health Foundation in Oklahoma City.
Co-investigators for the grant are Veronica Galvan Hart, Ph. Willard Freeman, Ph. D., co-director of the Center for Geroscience and Healthy Brain Aging, and Willard Freeman, Ph. D., professor of biochemistry and physiology at the OU College of Medicine. D., a researcher at the Oklahoma Medical Research Foundation. OMRF researcher Benjamin Miller, Ph. D., is also a collaborator.
About this research on inflammation and cognitive decline
Author: April Wilkerson
Source: University of Oklahoma
Contact: April Wilkerson – University of Oklahoma
Image: The image is credited to Neuroscience News
