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.
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.
DAPPD suppressed neuroinflammation and preserved cognition in mouse models of amyloidosis, suggesting potential for treating Alzheimer’s disease.
In a mouse tauopathy model, knocking out the NLRP3 inflammasome prevented toxic tau from forming.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Biogen researchers claim the antibody worked in people who got enough of it. To other researchers, the signal validates the amyloid hypothesis and injects fresh energy into the field. But is this interrupted dataset enough to approve?
The same endothelial cell response is found in various models of brain disease.
Prior research has focused on microglia interacting with synapses. New data show they also deal directly with the neuronal cell body. Like little conference rooms, specialized junctions host this communication.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
Cataloguing enhancer-promoter interactions in the four major cell types of the brain, researchers found that Alzheimer’s risk variants predominantly appeared in microglial enhancers.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.