Researchers have found a potential treatment for polycystic kidney disease, a genetic disorder that causes the kidneys to swell with multiple cysts and can eventually lead to organ failure.
The study published in the journal Nature Communications shows an approximately 50 per cent reduction in kidney size in afflicted mice following treatment.
The drug is now in early clinical trials on human subjects, the researchers said.
Autosomal dominant polycystic kidney disease (ADPKD) affects about 12 million people worldwide, with half developing end-stage kidney disease by the age of 60, according to the study.
“Once the kidneys have failed, the only options for survival are dialysis or a kidney transplant, a large percentage of ADPKD patients on dialysis die each year while waiting for a donated kidney,” said Indian origin researcher and study senior author Vishal Patel, Associate Professor at the University of Texas Southwestern Medical Centre.
According to the study, the new treatment showed no evidence of toxicity in animals or human cell tests. It is preferentially delivered to kidneys rather than the liver after being administered.
“We earlier showed that levels of a tiny RNA fragment called microRNA-17 are increased in models of ADPKD.
“MicroRNA-17 interferes with the normal function of other, beneficial RNAs, causing kidney cysts to grow. RGLS4326, as the new drug is called in development, works by blocking the harmful microRNA-17,” Patel added. (IANS)
While obesity is primarily associated with weight gain, a new study suggests it triggers inflammation in the nervous system that could damage important regions of the brain.
Developments in MRI, like diffusion tensor imaging (DTI), a technique that tracks the diffusion of water along the brain’s signal-carrying white matter tracts, have enabled researchers to study this damage directly.
“Brain changes were found in obese adolescents related to regions responsible for control of appetite, emotions and cognitive functions,” said study co-author Pamela Bertolazzi from the University of Sao Paulo in Brazil.
The World Health Organisation (WHO) data indicates the number of overweight or obese infants and young children increased from 32 million in 1990 to 41 million in 2016 globally.
For the study, researchers compared DTI results in 59 obese and 61 healthy adolescents, aged 12-16 years.
From DTI, the researchers derived a measure called fractional anisotropy (FA), which correlates with the condition of the brain’s white matter. A reduction in fractional anisotropy is indicative of increasing damage in the white matter.
The results showed reduction of FA values in the obese adolescents in regions located in the corpus callosum, a bundle of nerve fibre that connects the left and right hemispheres of the brain.
Decrease of fractional anisotropy was also found in the middle orbitofrontal gyrus, a brain region related to emotional control and the reward circuit. None of the brain regions in obese patients had increased fractional anisotropy.
According to researchers, this pattern of damage correlated with some inflammatory markers, like leptin, a hormone made by fat cells that helps regulate energy and fat stores.
In some obese people, the brain doesn’t respond to leptin, causing them to keep eating despite adequate or excessive fat stores. This condition, known as leptin resistance, makes the fat cells produce even more leptin.
Worsening condition of the white matter was also associated with levels of insulin, a hormone produced in the pancreas that helps regulate blood sugar levels. Obese people often suffer from insulin resistance.
“Our maps showed a positive correlation between brain changes and hormones, such as leptin and insulin,” Bertolazzi said.