A new study provides the first solid evidence for a loss-of-function mechanism in ALS caused by C9ORF72 repeat expansions.
In cognitively normal people with Aβ accumulation, tau pathology tracked along neurons from the hippocampus into the cortex and associated with poorer memory.
Crosstalk between different glia controls wiring in the developing brain.
Pathological forms of tau wander into presynaptic terminals, where they bind synaptogyrin-3. This cross-links synaptic vesicles, and mayhem ensues.
Both problems affect similar genes, but their expression changes in opposite directions.
A Japanese company enters the arena with a plasma Aβ test that rivals CSF for detecting brain amyloid.
In AIBL, memory declines as people with brain amyloid age. Without amyloid, episodic memory keeps steady, even in ApoE4 carriers.
Cryoelectron tomography yields pictures suggesting that poly-Gly-Ala peptide repeats form proteasome-trapping ribbons inside neurons.
Mutations spur fibrillization, while methylation and autophagy keep droplets nice and fluid.
Pinching the Aβ spigot with BACE1 inhibition doesn’t shrink plaques. It does slow their growth and stops new ones from forming. Is that going to be good enough?
Using a new fluorescent sensor, researchers recorded temperatures close to 50°C in these cellular energy plants.
The trial’s sponsor announced an early end to the large Alzheimer’s prevention study based on an interim futility analysis.
The more risk variants in a person’s genome, the faster they decline on both cognitive and motor tests.
Antibody comes close, but can’t slow mild AD.
In ADNI, only a handful of variants associate with amyloid PET. Their impact may vary by disease stage.