A slight drop in hospital admissions after amyloid PET, especially in people with positive scans, fell well short of the prespecified endpoint. Still, IDEAS is broadening into a research platform, and IDEAS 2 will add racial diversity.
In updating their broad evaluation of the risk literature, the commission blamed three more modifiable factors for causing 6 percent of all dementia, concluding that 40 percent of cases can be prevented.
Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.
New research pushes back the age at which dementia risk from cardiovascular and metabolic factors begins. Should protective lifestyle interventions start in youth?
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
Early data suggest that CT1812 and AL001 shift biomarker levels in Alzheimer’s disease and frontotemporal dementia, respectively. BI 425809 fails to improve cognition.
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
In the mouse retina, these tender threads connect pericytes on nearby capillaries. They enable cells to coordinate constriction and dilation of blood vessels in response to neuronal activity.
In female mice it’s the other X chromosome, not lack of a Y, that extends life and preserves memory in the face of amyloidosis. A histone demethylase gene partly explains this. It protects people, too.
The first high-resolution look at LRRK2 implies that pathogenic mutations increase binding to microtubules by biasing the kinase domain toward a closed, active conformation.