In a fly model of neurodegeneration, CDK5 slams autophagy, which leads to a runaway immune response that shoves aging neurons over the edge.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
Regulatory T cells rush into the brain after a stroke, quelling astrocytosis and aiding neural recovery.
A flavonoid reportedly spices up oxidative phosphorylation in microglial mitochondria, revving up phagocytosis of amyloid plaques in mouse models. The small study needs independent replication.
Liquid beads of TDP-43 form independently of stress granules and sequester proteins needed for nucleocytoplasmic transport.
Perturbations in the hormone correlate with memory problems. But does FGF23 act in the brain, or affect cognition indirectly via the kidneys?
Using rigorous tissue-processing techniques, researchers find thousands of newborn neurons in older human hippocampi, but a dearth in brains with AD pathology.
Blocking the receptor clears toxic proteins and improves memory in old mice. The work proposes a new role in microglia for a well-known B-cell receptor.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
The effect is small and stable, but consistent across several drugs. Researchers at CTAD debated whether it might be manageable by adjusting dosing.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.