Tau Snapshots from Neuroscience 2017
Novel ways to control tau captured the imaginations of scientists at the Society for Neuroscience annual meeting.
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Novel ways to control tau captured the imaginations of scientists at the Society for Neuroscience annual meeting.
The Alzforum team compiles some of their favorite stories from the past year.
At SfN 2017, some of the lesser-known tau toxicities came in for deep scrutiny.
Bayesian adaptive Phase 2 trial of anti-protofibril Aβ antibody did not, as desired, deliver an accelerated result. It will now continue to its end at 18 months.
Screen identifies antibody that induces mouse bone marrow cells to differentiate and travel to the brain, where they clear plaques.
Microglia-like cells from blood monocytes facilitate large-scale studies.
Initial report touted positive exploratory results for nelotanserin, but a correction wiped out optimism.
Using whole-genome sequence analysis, researchers find genetic variants linked to white-matter integrity, and cerebral and hippocampal volume.
In ADNI, only a handful of variants associate with amyloid PET. Their impact may vary by disease stage.
In AIBL, memory declines as people with brain amyloid age. Without amyloid, episodic memory keeps steady, even in ApoE4 carriers.
Researchers improve word recall by jolting the lateral temporal cortex, claiming this counters firing patterns linked to poor memorization.
Newly found labile cross-β filament structures may mediate multivalent protein interactions among low-complexity domains.
Its Challenge Network seeks to attract new investigators and new ideas to focus on cross-disease cell biology.
First presented at CTAD 2017, results suggest good safety, hint at efficacy for this serotonin-targeted drug.
A variant squelching expression of PAD4 enzyme reportedly drives up ALS risk by reducing aggregation of RNA-binding proteins.