Futility analysis predicts failure to reach primary endpoint.
Researchers consider the data encouraging, though questions linger about the cognition results. Did regulators mess up the randomization of this trial?
Herpes viruses that are commonly found in human brain promote rapid Aβ fibrillization and deposition in AD model systems.
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.
First look at substrate interactions reveals similarities but some surprises.
The latest effort to determine if a non-steroidal anti-inflammatory drug protects against Alzheimer’s posted negative results. Time to abandon the approach?
Aging lymphatic vessels in the meninges hinder waste clearance from the brain and exacerbate Aβ build-up.
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
Big data analyses correlate viral load with clinical, molecular, and pathological features of AD. Time to consider the pathogen hypothesis anew?
The material, previously used to treat children with growth deficiencies, triggered amyloid deposition in transgenic mice.
Are high-molecular-weight, multi-protease complexes cellular Aβ factories?
When the agency sent warning letters to 17 companies that falsely advertised cures and preventions for AD, most took down exaggerated claims. But can regulations stay ahead of the market?
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.
Chronic inhibition of protein synthesis, and slowing the dispersal of stress granules, contribute to neurodegeneration in C9ORF72 ALS/FTD.
In a fly model, C9ORF72 pathology pulls TDP-43 from the nucleus, which leads to disrupted nuclear import and neurodegeneration.