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.
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.
Removing senescent cells from mouse brain ameliorates the effects of mutant human tau.
A Wnt pathway inhibitor rescued dendritic spines in cultured neurons and cleared plaques in an AD mouse model.
X-ray crystallography yields high-resolution structure.
In AD brain, scientists see a genome-wide histone acetylation pattern replete with peaks near familiar AD genes such as APP, presenilin, tau, complement receptor, and more.
Much like tau, Aβ, and α-synuclein, pathological TDP-43 spreads through the mouse brain, following the trail of neuronal connections and corrupting healthy protein along the way.
Case study in early onset AD finds PET ligand tracks regional tau burden.
A new technique helps researchers single out and characterize toxic aggregates of TDP-43 from human brain.
Multiplexed marker analysis in single cells from human brain corroborates expression data, identifies microglia subsets in human brain.
Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.