Biogen/Eisai Halt Phase 3 Aducanumab Trials
Futility analysis predicts failure to reach primary endpoint.
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Futility analysis predicts failure to reach primary endpoint.
Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
Desikan pioneered advances in neuroimaging and neurogenetics, and was known for his passion and collaborative spirit.
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?
In mice, the back of the brain, near the neck, contains lymphatic vessels that are specialized to take up cerebrospinal fluid and deliver it to cervical lymph nodes.
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
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?
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.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
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.