Researchers publish 14 new AD variants. This includes one near WWOX, a gene that encodes a protein linked to tau and lipid metabolism.
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
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.
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.
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.