Anti-amyloid Alzheimer’s drugs show no clinically meaningful effect
Peer-Reviewed Publication
In honor of Alzheimer's Awareness Month, we’re exploring the science and stories surrounding Alzheimer’s disease.
Updates every hour. Last Updated: 16-Apr-2026 08:15 ET (16-Apr-2026 12:15 GMT/UTC)
Drugs that target amyloid beta proteins in the brain likely have no clinically meaningful positive effects, while increasing the risk of bleeding and swelling in the brain, a new Cochrane review has found.
In complex diseases, many different genetic changes can push cells into the same harmful state, as is the case with melanoma drug resistance. A new platform, PerturbFate, reveals how diverse genetic perturbations funnel into shared disease states, unlocking targets for new therapies. Next, the team plans to move this approach from cultured cells into living models to study aging and Alzheimer’s.
Northwestern University psychologist Andrea Russell sees older adults with early cognitive impairment riddled with anxiety. Some worry a missed word or forgotten appointment could signal Alzheimer’s disease. Others fear making a mistake in public. Some are too afraid to ask their doctor. Witnessing that uncertainty, and the stigma surrounding dementia, inspired Russell to spearhead a new Northwestern Medicine survey that found a vast majority of older adults would be willing to take a biomarker blood test to assess their Alzheimer’s risk.
Every thought, memory, and feeling we experience depends on trillions of tiny connection points in the brain called synapses. These are the junctions where one neuron passes signals to another, forming the vast communication network known as the connectome—the brain’s wiring diagram. Although scientists have developed powerful tools to increase or decrease neural activity, directly redesigning the brain’s physical wiring has remained far more difficult.
A research team led by Dr. LEE Sangkyu and Director C. Justin LEE at the Center for Memory and Glioscience within the Institute for Basic Science (IBS), in collaboration with Dr. LEE Kea Joo of the Korea Brain Research Institute (KBRI), has now developed a molecular tool that makes such structural editing possible. The new platform, called SynTrogo (Synthetic Trogocytosis), enables researchers to induce astrocytes to selectively remodel synaptic connections in a targeted brain circuit.