Here are the top medical news for the day:
Fat Transport Deficiency Unveiled as Key Factor in Rare Childhood Metabolic Crises
Researchers studying a protein linked to a rare, severe disease have made a discovery that sheds light on how cells meet their energy needs during a severe metabolic crisis. The findings could lead to new treatments for the disease and open new avenues of research for other conditions involving impaired fat metabolism.
Scientists at the Centre for Genomic Regulation (CRG) in Barcelona first identified a handful of protein-coding genes called TANGO in 2006. In 2016, the researchers found that mutations in TANGO2 causes a rare disease now officially recognised as TANGO2 Deficiency Disorder (TDD).
In the latest study, published in the Journal of Cell Biology, the researchers demonstrate that TANGO2 directly binds to a key fat molecule called acyl-CoA, transporting them like a shuttle inside cells. The authors of the study made the findings by tagging TANGO2 with glowing markers to trace its movements in live cells.
“Families sometimes only find out their child has TANGO2 deficiency only after a dramatic incident,” says ICREA Research Professor Vivek Malhotra, senior author of the study who first discovered the TANGO family of genes two decades ago. “One moment, everything seems normal. Then, under an energy-demanding situation, these children’s muscles and hearts fail to keep up.”
One of the few existing treatments for the condition involves giving patients high doses of Vitamin B5, an essential nutrient known to generate Coenzyme A
Though TANGO2 deficiency is rare, the science behind how cells shuttle fat to fuel-hungry tissues might apply more broadly. “It could help us understand heart or muscle diseases in the general population,” says Dr. Malhotra. “Millions of people wrestle with heart problems or abnormal fat metabolism, and the fundamental chemistry isn’t all that different. The biology of rare diseases can help us understand human health in general.”
Ref: Agustin Leonardo Lujan, Ombretta Foresti, Jose Wojnacki, Gonzalo Bigliani, Nathalie Brouwers, Maria Jesus Pena, Stefania Androulaki, Tomomi Hashidate-Yoshida, Maria Kalyukina, Sergey S. Novoselov, Hideo Shindou, Vivek Malhotra; TANGO2 is an acyl-CoA binding protein. J Cell Biol 5 May 2025; 224 (5): e202410001. doi: https://doi.org/10.1083/jcb.202410001
Virtual Reality Takes a Sweet Turn: New Device Lets You Taste Cake
Novel technology intends to redefine the virtual reality experience by expanding to incorporate a new sensory connection: taste.
The interface, dubbed ‘e-Taste’, uses a combination of sensors and wireless chemical dispensers to facilitate the remote perception of taste – what scientists call gustation. These sensors are attuned to recognize molecules like glucose and glutamate — chemicals that represent the five basic tastes of sweet, sour, salty, bitter, and umami. Once captured via an electrical signal, that data is wirelessly passed to a remote device for replication.
The study is published in the journal Science Advances.
“The chemical dimension in the current VR and AR realm is relatively underrepresented, especially when we talk about olfaction and gustation,” said Jinghua Li, co-author of the study and an assistant professor of materials science and engineering at Ohio State. “It’s a gap that needs to be filled and we’ve developed that with this next-generation system.
Despite the difficulty involved in replicating similar taste sensations for a majority of people, researchers found that in human trials, participants could distinguish between different sour intensities in the liquids generated by the system with an accuracy rate of about 70%.
While these results open up opportunities to pioneer new VR experiences, this team’s findings are especially significant because they could potentially provide scientists with a more intimate understanding of how the brain processes sensory signals from the mouth, said Li
lans to enhance the technology revolve around further miniaturizing the system and improving the system’s compatibility with different chemical compounds in food that produce taste sensations. Beyond helping to build a better and more dynamic gaming experience, the study notes that the work could be useful in promoting accessibility and inclusivity in virtual spaces for individuals with disabilities, like those with traumatic brain injuries or Long Covid, which brought gustatory loss to mainstream attention.
Ref: Shulin Chen et al. A sensor-actuator–coupled gustatory interface chemically connecting virtual and real environments for remote tasting.Sci. Adv.11,eadr4797(2025).DOI:10.1126/sciadv.adr4797
Scientists Uncover Mechanism Behind Retinoic Acid's Effectiveness in Treating Neuroblastoma
Neuroblastoma is a solid tumor that occurs in children. When high-risk, the disease has a poor prognosis. Decades ago, adding the drug retinoic acid to neuroblastoma treatment increased survival by 10-15%. However, this effect was only evident in post-chemotherapy consolidation after bulky primary tumors had largely been eliminated.
A recent study has shown that retinoic acid uses a novel mechanism to kill metastasized neuroblastoma. The drug “hijacks” a normal developmental pathway to trigger cancer cell death. The findings, which have implications for future combination therapy approaches, were published in Nature Communications.
“We’ve come up with an explanation for a decades-long contradiction about why retinoic acid works in post-chemotherapy consolidation but has little impact on primary neuroblastoma tumors,” said senior co-corresponding author Paul Geeleher, PhD, St. Jude Department of Computational Biology. “Retinoic acid’s activity heavily depends on the cellular microenvironment.
Metastasized neuroblastoma cells often migrate to bone marrow, where the bone morphogenetic protein (BMP) pathway signaling is highly active. The researchers showed that BMP signaling makes neuroblastoma cells much more vulnerable to retinoic acid.
Unexpectedly, we found that cells expressing genes from the BMP signaling pathway were very sensitive to retinoic acid,” said co-first and co-corresponding author Min Pan, PhD, St. Jude Department of Computational Biology. “However, since the bone marrow microenvironment causes neuroblastoma cells there to have higher BMP activity, it neatly explained why retinoic acid is very effective at treating those cells during consolidation therapy, but not the primary tumors during up-front treatment.
We found that, in neuroblastoma, BMP signaling works with retinoic acid signaling in the same way as during development,” said co-first author Yinwen Zhang, PhD, St. Jude Department of Computational Biology. Zhang characterized how transcription factors, the proteins that bind DNA to regulate gene expression, led to different results in highly retinoic acid-sensitive or insensitive neuroblastoma cells. “If there are a lot of BMP-signaling pathway transcription factors already on DNA, then retinoic acid signaling combines with it to promote downstream cell death–related gene expression. This occurs both in normal embryonic development and neuroblastoma cells in certain microenvironments.”
Ref: Pan, M., Zhang, Y., Wright, W.C. et al. Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid. Nat Commun 16, 2036 (2025). https://doi.org/10.1038/s41467-025-57185-y
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