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Fat cells steer flies away from pathogen-tainted food through a newly revealed neural circuit

If humans or animals eat something that causes them to feel unwell, they subsequently avoid this food source. Until now, it has been unclear precisely how this avoidance learning takes place. A new study shows that communication between the brain cells and fat cells could play a crucial role here. The participants from the Universities of Bonn and Tohoku (Japan) and University Hospital Bonn have revealed the previously unknown mechanism in the fruit fly Drosophila. It may also exist in a similar form in mammals and even in humans. The results have now been published in the journal Neuron.

Anyone who’s ever had an upset stomach after eating a bad meatball knows just how much this experience can put you off them. Within research, this is also known as “conditioned taste aversion”: The brain registers the immune response to the bacteria and their toxins and concludes from this that the food source should be avoided in the future.

It is not yet known how the immune system’s discovery of the pathogens leads to a change in behavior. “As this learned food avoidance can be found in all species, we investigated this question in a model organism – the fruit fly Drosophila,” explains Prof. Dr. Ilona Grunwald Kadow. “Within this model, we can clarify how the brain and body interact with each other to trigger an avoidance reaction that is vital for survival.”

Phage Therapy Gains Momentum in Antibiotic Resistance

As antimicrobial resistance continues to challenge traditional treatment protocols, bacteriophage therapy is emerging as a viable precision medicine alternative. Recent clinical developments demonstrate the potential of these virus-based interventions to target multi-drug resistant pathogens while preserving the host microbiome.


Growing antimicrobial resistance is prompting renewed interest in phage therapy, with preliminary data indicating improved outcomes when combined with standard antibiotics.

Fat-producing enzyme may amplify damage in Parkinson’s disease

As the flies aged, they developed Parkinson’s-like symptoms – including impaired movement and loss of brain cells – mirroring key aspects of disease progression seen in humans.

Using large-scale genetic screening made possible by the fruit fly model, the researchers systematically identified genes involved in α-synuclein-induced toxicity. Among these, the gene mino stood out for its strong effects on disease-related symptoms, leading the team to investigate its role further. This gene codes for the enzyme glycerol-3-phosphate acyltransferase (GPAT) and plays a key role in regulating fat metabolism in cells.

When the scientists reduced the activity of the mino gene, the flies experienced less loss of brain cells, improved movement, and healthier activity patterns. In contrast, increasing the gene’s activity worsened the flies’ symptoms.

The researchers then explored whether blocking GPAT could help counter these toxic effects. They tested a compound called FSG67, which blocks the activity of GPAT and has previously been studied in laboratory settings for obesity-related and metabolic disorders.

When the flies were treated with FSG67, the harmful effects of α-synuclein – including protein clumping and fat damage – were reduced. The scientists observed similar protective effects in mouse brain cells grown in the laboratory.

Going forward, the scientists will focus on further validating these findings and exploring the possibility of developing GPAT inhibitors as a new class of drugs for Parkinson’s disease. ScienceMission sciencenewshighlights.


3 Interventions to Show Aging is Treatable: The US Government’s $38M Bet

The US Government is finally treating aging as a modifiable condition. Discover the VITAL-H trial: a $38M federal study testing Rapamycin, Semaglutide, and Dapagliflozin to set the first FDA-approved roadmap for healthy longevity.
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Is aging finally becoming a recognized medical priority? In this video, we break down the historic VITAL-H trial, a $38 million initiative funded by ARPA-H (the \.

A black licorice compound slashes gut inflammation and cell death in IBD models and animals

A new study published in Stem Cell Reports demonstrates how a human stem cell-derived model of the intestine can be used to identify potential therapies for inflammatory bowel disease (IBD), highlighting glycyrrhizin as a promising candidate for reducing intestinal inflammation and cell death.

The burden of IBD is rising globally, with an estimated 4 million people affected worldwide. The disease is characterized by chronic inflammation of the intestinal wall, leading to symptoms such as persistent diarrhea, abdominal pain, and fatigue. Standard treatments include anti-inflammatory drugs and other immune-targeting therapies, but many patients experience only limited benefit.

High-throughput screening (HTS) offers a promising strategy to discover new IBD therapies but depends on having a reliable model of the human intestinal wall for laboratory testing.

A transcriptional atlas of the pubertal human growth plate reveals two populations of stem cells and direct effect of growth hormone

This study reveals two populations of cartilage stem cells in both human and mouse growth plates, reshaping our understanding of longitudinal growth.

Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders

Mitochondria make essential contributions to neural development. Zhao and colleagues provide an overview of the mechanisms that regulate mitochondrial biogenesis, degradation, remodelling and transport, the importance of these processes for neural development and the proposed links between altered mitochondrial dynamics and neurodevelopmental disorders.

CT and MRI LI-RADS Treatment Response Assessment 2024: Core Concepts for Clinical Practice

Post-treatment HCC imaging just got clearer. The updated 2024 LI-RADS TR algorithm refines criteria for radiation vs non-radiation therapies and adds MRI features to better detect viable tumor, key for accurate response assessment and management.


Multiple locoregional therapies are available for HCC, with imaging findings specific to each modality. The updated 2024 CT and MRI LI-RADS TR assessment criteria provided distinct algorithms for use after nonradiation or radiation-based therapies, simplified the definition of viable disease, and incorporated MRI ancillary features to enhance detection of tumor viability. These updated criteria can improve diagnostic accuracy, resulting in more effective clinical management of HCC.

Confirmed precursor to commonest form of esophageal cancer offers opportunities to catch the disease early

Scientists have found the strongest evidence to date that a condition known as Barrett’s esophagus is the starting point for all cases of esophageal adenocarcinoma—the most common type of esophageal cancer in the developed world—even when telltale signs of this pre-cancerous stage are no longer visible. The findings, published in Nature Medicine, could help improve screening for and early detection of esophageal cancer, the sixth-most deadly cancer, helping improve outcomes for the disease.

Cancer of the esophagus, including its most common form, esophageal adenocarcinoma (OAC), is on the rise in Western countries. It is difficult to treat because it is often caught at an advanced stage, when treatment options are limited. Scientists and doctors have known for some time that the development of esophageal cancer is linked with Barrett’s esophagus, which shows up in endoscopy as a pink patch on the surface of the esophagus. Barrett’s esophagus affects around one out of every 100 to 200 people in the United Kingdom.

Between three and 13 people out of 100 with Barrett’s esophagus will go on to develop esophageal adenocarcinoma in their lifetime. However, around half of OAC patients have no detectable Barrett’s esophagus when their cancer is found, raising doubts about whether it is always the precursor.

Abstract: Offering a topical strategy in skin cancer

https://doi.org/10.1172/JCI189044 Brian C. Capell & team identify the epigenetic regulator LSD1 as critical for epidermal development and find its inhibition suppresses tumors in two cutaneous squamous cell carcinoma mouse models by promoting immunosurveillance.

The image shows immunofluorescence from mice lacking LSD1 in the skin, revealing profound activation of cutaneous retinoid signaling (as measured by CRABP2 levels in green); keratin 14 (red); nuclei (blue).


1Department of Dermatology and.

2Penn Epigenetics Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.

3Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.

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