At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.
Two groups create mice for imaging and manipulation of microglia, leaving related cells untouched. The trick? Piggybacking on Tmem119 expression.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
Today, the creators of bioRχiv launch a repository for preliminary medical research, including clinical trial data.
Microglial responses to Alzheimer’s risk variants, and to tau pathology, appear to show a sex difference. Microglia in male versus female mice use different biological mechanisms to maintain homeostasis.
At a joint Keystone symposia, researchers reported how microglia, via TREM2, compress plaques and rein in the pathogenic distortion of neurites into swollen stubs. Without TREM2, these damaged neuronal processes served as fertile ground for tau propagation.
At Keystone, researchers described how directly converting astrocytes into neurons within the mouse striatum restored neuron numbers in a model of PD.
Brains of old mice birth fewer neurons when T cells invade the subventricular zone. The immune cells spew inflammatory cytokines that snuff out neurogenesis.
Null results ended the development of the neuroprotective drugs edonerpic and abeotaxane, the AMPA receptor modulator S47445, and the dietary formulation tricaprilin.
Drug didn’t slow decline in a Phase 2 trial.
Through an endocytic process called LANDO, microglia clear β-amyloid and route their used Aβ receptors, including TREM2, back to the plasma membrane. Without it, aggregates pile up outside and form plaques.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
TREM2 required for reduction of plaque load in CD33 knockouts.
Injecting α-synuclein fibrils into mouse gut sparked the proteopathic spread of misfolded α-synuclein into the brain, where the aggregates killed dopaminergic neurons and caused motor problems.