CryoEM helps explain how the inhibitory receptors open and close their ion channels.
Regulatory T cells rush into the brain after a stroke, quelling astrocytosis and aiding neural recovery.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
By crossing 5XFAD mice with multiple different reference strains, scientists make genetically diverse AD mice to better mimic human late-onset disease.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
By marrying iPSCs, human genomic data, and analysis of postmortem tissue, researchers tied loss of GABAergic signaling to tauopathies such as FTD and PSP, but not AD.
Multiplexed marker analysis in single cells from human brain corroborates expression data, identifies microglia subsets in human brain.
Disrupting circadian clocks in astrocytes and microglia unleashed harmful responses in these glial cells, leading to neuronal damage.
A new technique helps researchers single out and characterize toxic aggregates of TDP-43 from human brain.
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.
Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
At SfN, some scientists described how circulating immune cells deliver aging to the mouse hippocampus; others held off parkinsonism by blocking the effects of eotaxin’s rise in blood. Human trials are starting.
The material, previously used to treat children with growth deficiencies, triggered amyloid deposition in transgenic mice.
Case study in early onset AD finds PET ligand tracks regional tau burden.
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.