Toggle light / dark theme

Drug combination sidesteps resistance in aggressive childhood neuroblastoma models

A discovery from Australian researchers could lead to better treatment for children with neuroblastoma, a cancer that currently claims 9 out of 10 young patients who experience recurrence. The team at the Garvan Institute of Medical Research in Sydney, Australia, found a drug combination that can bypass the cellular defenses these tumors develop that lead to relapse.

In findings made in animal models and published today in Science Advances, Associate Professor David Croucher and his team have shown that a drug already approved for other cancers can trigger neuroblastoma cell death through alternative pathways when the usual routes become blocked. This discovery could lead to better treatment strategies for children whose cancers have stopped responding to standard chemotherapy.

Neuroblastoma is the most common solid tumor in children outside the brain, developing from nerve cells in the adrenal glands above the kidneys or along the spine, chest, abdomen or pelvis. It is typically diagnosed in children under 2 years old. While those with low-risk disease have excellent outcomes, around half of patients are diagnosed with high-risk neuroblastoma—an aggressive form where tumors have already spread. Of these high-risk patients, 15% don’t respond to initial treatment, and half of those who do respond will see their cancer return.

Metabolomic Investigation of Blood and Urinary Amino Acids and Derivatives in Patients with Type 2 Diabetes Mellitus and Early Diabetic Kidney Disease

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease; however, few biomarkers of its early identification are available. The aim of the study was to assess new biomarkers in the early stages of DKD in type 2 diabetes mellitus (DM) patients. This cross-sectional pilot study performed an integrated metabolomic profiling of blood and urine in 90 patients with type 2 DM, classified into three subgroups according to albuminuria stage from P1 to P3 (30 normo-, 30 micro-, and 30 macroalbuminuric) and 20 healthy controls using high-performance liquid chromatography and mass spectrometry (UPLC-QTOF-ESI MS). From a large cohort of separated and identified molecules, 33 and 39 amino acids and derivatives from serum and urine, respectively, were selected for statistical analysis using Metaboanalyst 5.0. online software.

How a gene shapes the architecture of the human brain

Researchers around the world are studying how the human brain achieves its extraordinary complexity. A team at the Central Institute of Mental Health in Mannheim and the German Primate Center—Leibniz Institute for Primate Research in Göttingen has now used organoids to show that the ARHGAP11A gene plays a crucial role in brain development. If this gene is missing, key processes involved in cell division and structure become unbalanced.

The human brain distinguishes us from other living beings like no other organ. It enables language, abstract thinking, complex social behavior, and culture. But how can this extraordinarily powerful organ develop, and how is it ensured that nerve cells and supporting cells form in exactly the right places to create the complexity of the human brain?

A team led by Dr. Julia Ladewig at the Central Institute of Mental Health (CIMH) in Mannheim and Dr. Michael Heide at the German Primate Center (DPZ) in Göttingen has investigated this question at the molecular level.

Your body may already have a molecule that helps fight Alzheimer’s

Spermine, a small but powerful molecule in the body, helps neutralize harmful protein accumulations linked to Alzheimer’s and Parkinson’s. It encourages these misfolded proteins to gather into manageable clumps that cells can more efficiently dispose of through autophagy. Experiments in nematodes show that spermine also enhances longevity and cellular energy production. These insights open the door to targeted therapies powered by polyamines and advanced AI-driven molecular design.

Aging Scrambles Brain Proteins — And Diet Could Partly Reverse It

As we get older, our brains start to change in ways that make them increasingly vulnerable to disease – and a detailed new study of these changes points to a way some of this wear and tear might be prevented or reversed.

Researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute in Germany used mass spectrometry to analyze the balance of brain proteins in both young and old mice, finding differences in a process called ubiquitylation as the animals aged.

Ubiquitylation adds chemical tags to proteins, telling the brain which of these busy molecules are past their peak and should be recycled. In older mouse brains, the ubiquitylation tags really start to pile up on certain proteins.

A nonsurgical brain implant enabled through a cell–electronics hybrid for focal neuromodulation

MIT researchers have taken a major step toward making this scenario a reality. They developed microscopic, wireless bioelectronics that could travel through the body’s circulatory system and autonomously self-implant in a target region of the brain, where they would provide focused treatment.

In a study on mice, the researchers show that after injection, these miniscule implants can identify and travel to a specific brain region without the need for human guidance. Once there, they can be wirelessly powered to provide electrical stimulation to the precise area. Such stimulation, known as neuromodulation, has shown promise as a way to treat brain tumors and diseases like Alzheimer’s and multiple sclerosis.

Moreover, because the electronic devices are integrated with living, biological cells before being injected, they are not attacked by the body’s immune system and can cross the blood-brain barrier while leaving it intact. This maintains the barrier’s crucial protection of the brain.

A nonsurgical brain implant enabled through a cell–electronics hybrid for focal neuromodulation.


Photovoltaic devices attached to immune cells travel through the blood to inflamed brain regions.

/* */