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?
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.
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?
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.
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?
In a fly model, C9ORF72 pathology pulls TDP-43 from the nucleus, which leads to disrupted nuclear import and neurodegeneration.
Mutations that destabilize α-synuclein tetramers leave young mice with severe and progressive motor problems resembling those of PD.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
In a new take on mosaicism and Alzheimer’s, scientists claim that APP mRNAs convert into DNA and reinsert into the genome. Full of mutations, these “genomic cDNAs” crop up in aging and sporadic AD.