Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
After shutting down a Phase 3 program last March, Biogen now says the futility analysis it did was incorrect, and that a new analysis of a larger dataset in fact supports filing for FDA marketing approval next year.
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.
A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as Alzheimer’s.
DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
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.
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.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
GV-971, an oligosaccharide derived from marine kelp, was approved to treat AD in China. Preclinical studies suggest the drug soothes neuroinflammation by balancing the gut microbiome.
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.
Researchers induced cortical organoids to grow their own vasculature and even form a blood-“brain” barrier, making the little blobs more useful for studying disease.
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.