In the largest genetic study of Alzheimer’s disease, researchers at the School of Medicine and the University of California, San Francisco, have found that genes that increase risk of cardiovascular disease also heighten the risk for Alzheimer’s.
Using technology similar to what is found in many eye doctors’ offices, School of Medicine researchers have detected evidence suggesting Alzheimer’s in older patients who had no symptoms of the disease.
School of Medicine researchers have found that the pathways through which various types of brain cells are damaged by Alzheimer’s disease varies, depending on the genes involved. The findings are published in the journal Genome Medicine.
Sticky amyloid plaques play a role in Alzheimer’s disease. School of Medicine researchers have shown that an antibody targeting a minor part of the plaques – a protein known as APOE – can sweep away the damaging plaques, opening potential treatment options.
Researchers at the School of Medicine are getting a clearer picture of the connection between tau and amyloid beta, the two proteins at the heart of Alzheimer’s disease. Their insights may lead to new treatments.
Washington University School of Medicine researchers have found that circadian rhythm disruptions occur much earlier in people whose memories are intact but whose brain scans show early, preclinical evidence of Alzheimer’s.
A long-term study of adult children of Alzheimer’s patients — led by the School of Medicine — aims to define who is likely to develop the disease and when, and to establish a timeline for how quickly the disease will progress.
It has been another year of achievement at Washington University in St. Louis. Seniors Jasmine Brown and Camille Borders both were named Rhodes Scholars, graduate Lizzy Christ was named 2017 NCAA Woman of the Year and researchers discovered tomb of a Maya ruler, explored the link between sleep and Alzheimer’s and found that babies are master social statisticians in disguise. Here, The Record shares 2017’s most-read stories in The Source.
Chronic poor sleep has been linked to cognitive decline. A new study from the School of Medicine shows that a sleepless night causes levels of the Alzheimer’s protein amyloid beta to rise faster than the brain’s waste-disposal system can remove it. Persistently high levels of the protein can set off a cascade of brain changes leading to dementia.
School of Medicine researchers have identified a compound that targets the APOE protein in the brains of mice and protects against damage induced by the Alzheimer’s protein amyloid beta.