Bump in the Road or Disaster? BACE Inhibitors Worsen Cognition
The effect is small and stable, but consistent across several drugs. Researchers at CTAD debated whether it might be manageable by adjusting dosing.
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The effect is small and stable, but consistent across several drugs. Researchers at CTAD debated whether it might be manageable by adjusting dosing.
Regulatory T cells rush into the brain after a stroke, quelling astrocytosis and aiding neural recovery.
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.
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?
Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
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.
Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
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.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.
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.