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Tau oligomers ensnare an RNA-binding protein and its partner, a type of methylated RNA, in the cytosol of neurons. This triad stresses the cells, leading to neurodegeneration in mice. In people, tau draws in more methylated RNA as Alzheimer's pathology worsens.
Higher Aβ42 in these neurons correlated with greater plaque load and cognitive decline in their 53 donors, suggesting amyloid overproduction in sporadic AD.
Large study confirms that insufficient sleep correlates with amyloid accumulation in otherwise healthy adults. Too much sleep is also bad, but for different reasons.
North Carolina and South Texas centers to focus on risk factors and diversity.
Network analysis of human PET brain imaging data suggests amyloid plaques set the stage for microglial activation that, in turn, drives tangle spread through the brain.
Markers of neuronal injury rose in plasma within a few months of severe COVID-19, then fell back to normal by six months. Some cases with brain symptoms had lower Aβ and higher tau in their blood.
Aβ oligomers rev up glutamate release, depressing synapses for the long term. This instigates the pathological phosphorylation of tau.
Topline results from a Phase 2 trial of semorinemab suggest the therapeutic antibody may have eased the cognitive downturn in people with mild to moderate Alzheimer’s disease.
Decades before tangles become rampant, the biomarker p-tau231 rises in both CSF and plasma. More surprising: neuroinflammation markers do, too.
Among old people with high total tau levels in plasma, cognition slid far less in those who are active than in their inactive peers. Could blood tests motivate at-risk people to exercise?
Myelin breakdown in the Alzheimer’s brain is thought to be a consequence of plaques, but a new study in mice suggests it may be a cause.
AD risk scores based on gene expression in microglia associate with having amyloid plaques, and a microglial genomic atlas displays how variants influence gene expression. Polygenic variation in neurons sways cognition.
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
Single-nuclei expression analysis identified different cell clusters from people who carried autosomal-dominant Alzheimer’s mutations or risk variants for late-onset AD. Also, microglia RNA-Seq goes big.
Scientists are testing passive and active immunotherapies that take down pyroglutamate Aβ, and a combo Aβ/tau vaccine.
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