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.
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.
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.
DAPPD suppressed neuroinflammation and preserved cognition in mouse models of amyloidosis, suggesting potential for treating Alzheimer’s disease.
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
Hypertension in people as young as the mid-30s can predict late-life cerebrovascular disease and brain shrinkage. Intensive reduction of blood pressure can prevent the damage, but not when given in late life.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
In vicinity of plaques, astrocytes and glia change gene expression in concert.
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.