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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.”

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.


The subtle science behind safer brain implants

In a recent publication appearing in Advanced Science, researchers at the Netherlands Institute for Neuroscience challenge the assumptions surrounding the design and materials used for brain implants. Softer, flexible implants are gentler than older ones, but they are not completely harmless. By carefully studying these effects, researchers can begin to design safer implants, and bring long-term, reliable implants closer to reality.

In laboratories around the world, scientists are working on a bold goal: restoring blindness using brain implants. But behind the futuristic promise lies a quieter, more complicated story about materials, assumptions, and the limits of what we really understand about the brain.

One part of this story includes a deceptively simple question: How do you place a foreign object in the brain without evoking a reaction?

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.

Abstract: Implications for protecting against cognitive impairment following HeadInjury👇

Here, Michael T. Heneka & team find the inflammasome adaptor ASC drives long-lasting brain inflammation and cognitive problems after mild head injury in a closed-head injury model.

The figure shows skeletonized activated microglia (Iba1+ cells) following closed head injury, with mice lacking ASC show showing preservation of morphological features, particularly at later time points.


3Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Belvaux, Luxembourg.

4German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

5Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.

Abstract: Immune signaling and function in neurodegeneration:

Yvonne L. Latour & Dorian B. McGavern contribute a Review to the JCI Series on Neurodegeneration, discussing signaling pathways, cellular players, and immune responses shared across multiple neurodegenerative diseases, while considering external factors that may influence CNS disease progression. Neurodegeneration.


Viral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.

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