Researchers at the University of British Columbia and BC Cancer have developed a new way to target proteins long considered “undruggable,” opening the door to new treatments for prostate cancer and other serious diseases. Known as intrinsically disordered proteins, these molecular shapeshifters are extremely difficult to target with medication due to their flexible and ever-changing structure. They play a central role in a wide range of diseases—including cancer, neurodegenerative disorders, heart disease and autoimmune conditions—yet only a handful of medications currently exist that can target them. In a study published today in Nature Signal Transduction and Targeted Therapy, the researchers demonstrate a new approach for designing drugs that bind more strongly to these proteins and block their disease-causing activity. In some cases, the compounds they developed bound up to a million times more tightly than any previously reported.  

Gambling companies are reaching young men – the group most likely to exhibit problem gambling behaviour – on social media at more than double the rate of women, a study has found.

Cognitive decline in Alzheimer’s disease differs substantially from one person to the next and is not well predicted by existing medical tests. Among people with preclinical Alzheimer’s disease who began one of two related studies with no symptoms, researchers from the Keck School of Medicine of USC found three distinct patterns: stable, slow cognitive decline and fast cognitive decline. About 70% of participants remained stable over the study period of approximately six years. For the study, researchers analyzed data from the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease (A4) study, a clinical trial of the monoclonal antibody solanezumab. They also included data from the Longitudinal Evaluation of Amyloid Risk and Neurodegeneration Extension (LEARN), a companion study of people without the elevated levels of amyloid-beta in the brain which are an early sign of Alzheimer’s disease. Before and during the trial, participants completed a series of cognitive tests that measured their memory, attention and thinking. Scores on these tests were used to track their rate of cognitive decline. The researchers also collected brain scans and blood tests, including phosphorylated tau (P-tau217), a marker of the protein tau, one of the hallmarks of Alzheimer’s disease. Participants who showed a gradual or a fast decline had higher P-tau217 levels when the study began, as well as higher levels of tau on brain scans than those who remained stable. They also had a smaller hippocampus, an area of the brain linked to memory and one of the first affected by Alzheimer’s disease. Using biomarker data, the researchers could correctly predict whether participants were likely to stay stable or worsen about 70% of the time.