Gene Disruption Haunts Tau Mouse—Knock-Ins Look Promising
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.
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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.
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.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.
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.
Multiplexed marker analysis in single cells from human brain corroborates expression data, identifies microglia subsets in human brain.
By crossing 5XFAD mice with multiple different reference strains, scientists make genetically diverse AD mice to better mimic human late-onset disease.
Ever wonder why it’s so easy to nod off in a hammock? Turns out swaying back and forth improves sleep and even enhances memory in people.
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.