In presynapses, binding sequesters synaptic vesicles.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
First look at substrate interactions reveals similarities but some surprises.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
Absent the receptor, microglia ignore Aβ seeds and new plaques, which then absorb little ApoE and stay diffuse.
In a fly model of neurodegeneration, CDK5 slams autophagy, which leads to a runaway immune response that shoves aging neurons over the edge.
Cryo-EM 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.
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