Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
Lanabecestat, elenbecestat, and umibecestat all showed data at the AD/PD conference in Lisbon. Learn what definitely doesn’t work and what might yet.
Long recognized in dendrites, scientists now report that substantial synaptic proteome remodeling happens on the axonal side, too.
More mouse data add to the argument that a flashing light sequence could potentially fight cognitive decline.
The global agency’s report recommends physical activity, a healthy diet, stopping alcohol abuse and smoking, and managing one’s weight, blood pressure, and diabetes.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
At AD/PD 2019, scientists implicated both peripheral and central innate immunity in promoting propagation.
As data increasingly blame the microglia response as a driving force in Alzheimer’s disease, researchers are investigating whether tempering these cells will aid cognition.
An FDA-approved insomnia drug lengthened total sleep time in patients with mild to moderate Alzheimer’s, suggesting it might be able to lessen a troublesome symptom of the disease.
In the largest study yet to track tau via repeated PET scans, researchers found that tau pathology increased over baseline only in people with Aβ deposition. The more tau a person had at baseline, the more tau increased later on, and the more they slipped on cognitive tests.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
In ADNI, blood marker exposes ongoing neurodegeneration across disease stages.
Scientists propose that LATE is a neurodegenerative disease marked by TDP-43 pathology in limbic regions, and memory loss. After death, it can be seen alone or with other pathology.