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 link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
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.
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?
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
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.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
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.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.