Amyloid-PET Results Lead Some to Ponder Assisted Death in Future
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.
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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.
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.
The resource boasts 56 stem cell lines derived from tau mutation carriers, patients with sporadic disease, healthy controls, and engineered isogenic lines, including some that have their mutation corrected by CRISPR.
The rare ApoE3 Christchurch variant prevented tau tangles, neurodegeneration, and cognitive decline in a woman’s brain for decades, despite massive amyloid buildup from a familial presenilin AD mutation.
While former professional soccer players have less risk for heart disease and cancer than the general population, they are five times more likely to die with a neurodegenerative disease in old age.
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.