Does CSF Aβ Reflect Protofibril Concentration, Rather Than Plaques?
In mice, this marker correlated better with amyloid protofibrils in the brain than with plaques. So did CSF markers of neurodegeneration, highlighting the toxicity of protofibrils.
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In mice, this marker correlated better with amyloid protofibrils in the brain than with plaques. So did CSF markers of neurodegeneration, highlighting the toxicity of protofibrils.
Two studies tie repeated stretches of DNA to increased odds for AD. One encodes poly-GR peptides that aggregate.
Surveys of CSF proteins from the GENFI and ALLFTD genetic cohorts flag altered biological processes and point toward FTD fluid markers.
An endoplasmic reticulum protein helps lipids bud from this organelle. Knocking out the protein in microglia curtailed lipid droplets, and enhanced amyloid clearance.
A new super-resolution microscopy technique sheds light on synaptic dysfunction.
Mice have a small pool of such Tregs. Removing them hobbles the hippocampus, beckons immune invasion, revs glia, and quashes neurogenesis.
In AD mouse models, replacing ApoE3 with ApoE3Ch preserves memory.
The nod will allow people who have completed 18 months of biweekly IV dosing to transition to monthly IVs. An application for subcutaneous dosing is pending.
Triggered by oxidative stress, this degradation signal may protect neurons.
By tracking how mutations influence the incorporation of monomers, scientists pinpoint which residues shape tau fibrils.
In female mice, the silencing of several cognitive genes on maternally inherited X chromosomes correlated with poor memory; re-expressing the genes improved it.
In people with PD and other Lewy body diseases, α-synuclein accumulates in the kidneys, scientists say. In mice, it spreads from there to the brain.
New 3D model shows how a tau kinase and Apoe4 astrocytes kill neurons through oxidative stress.
Hyperconnectivity ushers tangles from temporal lobe to posterior cortex. Study could revive interest in trialing anti-convulsants with tau biomarkers as an outcome.
Cell survival factor EBP1 binds the enzyme’s presenilin subunit, interfering with APP binding and lowering Aβ output. EBP1 drops with age and in AD brains.