The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
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.
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.
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.
“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.
Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
A prospective progeria drug revs up cellular autophagy and clears tau in neurons derived from patients with frontotemporal dementia. In mouse models, the drug rescues abnormal behavior.
Senolytic drugs kill these cells, temper Aβ, and improve cognition in transgenic mice.
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.
Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.