Longitudinal and genetic studies reveal that intelligence underlies cognitive reserve.
Many genes that increase risk for late-onset AD are expressed in microglia, and researchers are going cell by cell to unravel the pathways involved in the immune response to amyloid and tau.
At SfN and in new papers, scientists describe how synapses crater under the combined onslaught of Aβ and tau. They also link gene-expression signatures to the selective vulnerability of excitatory neurons to tau pathology.
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.
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.
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.