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.
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.
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.
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?
Cognitive enrichment in early life correlated with less Alzheimer’s pathology, and slower cognitive decline, in late life.
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.
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.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
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.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.