This research shows that the sympathetic nervous system is disrupted at the earliest stages of ALS, despite sympathetic neurons themselves remaining intact. Early loss of signalling receptors may contribute to muscle degeneration and disease progression, identifying new opportunities for earlier diagnosis and therapies that preserve muscle function and improve patient outcomes.

This research reveals how Streptococcus evades immune attack by shedding its hair-like surface proteins, distracting immune cells while provoking excessive immune activation. The findings provide a new explanation for how recurrent strep infections can trigger autoimmune diseases and suggest treatments should target both the bacteria and the immune response.

This research introduces the first simple mathematical model capable of capturing the cooperative folding of alpha helices, a fundamental protein structure. By revealing how these proteins fold, stabilize, and misfold, the model offers new insights into diseases such as Alzheimer's and Parkinson's while providing a fast, flexible platform for protein research.

This research investigates how glutamine-rich regions within the LAG-3 protein influence Notch signaling, a critical pathway for cell communication and development. Using CRISPR gene editing, the study found that removing glutamine repeats alters stem cell behavior and cell-cycle progression, providing insights relevant to cancer, Alzheimer’s disease, and future therapies.

This research investigates how misfolded Islet Amyloid Polypeptide (IAPP), a protein associated with Type 2 diabetes, affects blood clot formation. Laboratory experiments showed that misfolded IAPP creates unusually dense and resilient clots. These findings may help explain elevated cardiovascular risk in diabetes and identify new targets for preventing heart attacks and strokes.

This research investigates the neurological causes of sleep dysfunction in people with myotonic dystrophy, a common multisystem muscular dystrophy. Using mouse models and brain activity monitoring, the study examines how diseased brains lose the ability to compensate for stress, providing new insights into sleep quality, cognition, and disease progression.

This research investigates the protein SLX4, a key coordinator of DNA repair. Using complementary techniques, it identifies 221 interacting proteins, most previously unknown. Findings reveal a complex network involved in genome maintenance, offering new insights into cellular repair mechanisms and improving understanding of diseases such as cancer.

This research explores how immune-related cells and molecules, beneficial in wound healing, may become harmful in Parkinson’s disease. Using the fruit fly as a model organism, the study investigates which inflammatory processes contribute to brain damage. Early results suggest that excessive activation worsens degeneration, offering potential targets for future therapies.

Electrical signals in the body depend on ion channels that regulate salt movement across cell membranes. When these channels malfunction, diseases like epilepsy and heart arrhythmias can occur. This research decodes how faulty ion channels work, revealing potassium-based mechanisms that could restore electrical signaling and guide new therapies.

Fruit flies normally die from sleep loss due to lethal gut inflammation. But a mutant “fumin” fly, which sleeps very little, survives without inflammation. This research investigates how altered dopamine processing protects these flies, offering insight into why sleep is essential and how sleep loss contributes to disease.