How errors in the “cell skeleton” lead to a smaller brain
Peer-Reviewed Publication
Updates every hour. Last Updated: 24-May-2026 09:15 ET (24-May-2026 13:15 GMT/UTC)
Why do some children develop a brain that is too small (microcephaly)? An international research team involving the German Primate Center – Leibniz Institute for Primate Research (DPZ), Hannover Medical School (MHH), and the Max Planck Institute of Molecular Cell Biology and Genetics has used human brain organoids to investigate how changes in important structural proteins in the cell lead to this severe developmental disorder (EMBO Reports).
Researchers compared the genomes of two dangerous bacteria, Escherichia coli (E. coli) and Klebsiella pneumoniae, isolated from blood and faecal samples from Tanzanian newborns admitted with fever. In the majority of cases the bacteria were almost genetically identical, suggesting that the same strain had moved from the gastrointestinal tract into the blood. There was also a bacterial strain that acquired an antimicrobial resistance (AMR) gene between the gut and the blood, a concerning development which limits treatment options.
These findings will support future diagnostic strategies since stool samples are far easier to collect from newborns than blood, allowing clinicians to identify infants at risk of developing sepsis. This development would be vital for very low birthweight babies or those in neonatal units where sepsis and AMR outbreaks can be deadly.
Arousal by the brainstem and subcortical regions, and awareness from cortical regions combine to produce consciousness in the brain. While arousal or wakefulness is regulated by the ascending reticular activating system of brainstem, the exact mechanism by which brainstem injuries lead to disorder of consciousness (DoC) remains unelucidated. Now, researchers reveal the roles of four nodes in the brainstem in DoC, and describe therapies targeting these nodes and their networks to aid recovery.
Maintaining long-term health has become a major challenge, driving research into ways to extend “healthspan” rather than lifespan alone. In a recent study, researchers from Japan investigated COX7RP, a mitochondrial protein that promotes the assembly of mitochondrial respiratory supercomplexes essential for efficient energy production. They found that boosting COX7RP improves mitochondrial performance, enhances metabolic health, and significantly prolongs lifespan in mice, opening doors to novel anti-aging interventions and therapeutic strategies for aging-related diseases.