Piezo1 Steers Microglia Toward Rigid Aβ Plaques
Without this mechanosensor, microglia slowly respond to plaques. In mice, a Piezo1 agonist bolstered plaque containment and lowered amyloid burden.
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Without this mechanosensor, microglia slowly respond to plaques. In mice, a Piezo1 agonist bolstered plaque containment and lowered amyloid burden.
Conformers amplified from CSF of late-stage PD adopt distinct folds and trouble neurons.
A new method reveals distinct synaptic states, some tied to amyloidosis, that were not seen in prior nuclear transcriptomic data.
Excitatory neurons from people who died with Alzheimer’s disease carried more mutations than did neurons from healthy controls. Do such variants contribute to the demise of neurons?
When this retromer faltered in mice, Aβ levels rose in the brain and synaptic signaling waned in the transentorhinal cortex. General retromer loss in hippocampal neurons evoked dystrophic microglia similar to those seen in AD.
In mice, oligomeric Aβ causes these macrophages to produce SPP1. Knocking out this pro-inflammatory cytokine quiets microglia and protects synapses.
Microglia within 10 micrometers of Aβ plaques expressed a disease-associated signature. Astrocytes rubbernecked from a bit farther away.
Live imaging of mouse brain reveals that microglia quickly engulf cell bodies while astrocytes dispose of the neuron’s more distal reaches. The cleanup crew tires with age.
Single-nucleus RNA-Seq of human brain finds regional differences in endothelial cell subtypes. Transcriptomes change in the presence of plaque or vascular amyloid.
People who carry the ApoE4 variant are more likely to succumb to the virus. In vitro, SARS-CoV-2 infects more ApoE4 than ApoE3 brain cells. Astrocytes were activated, neurons degenerated.
In mice, nixing ApoE4 from neurons squelched tau pathology, myelin loss, and neuronal death.
More evidence that presynaptic tau may spread from neuron to neuron.
In VSP35 knockout cells, surface proteins get trapped in endolysosomes. They swell with undigested proteins and APP, then spew their contents outside the cell.
In cells from people with Down’s syndrome, and in mouse models of DS and Alzheimer’s, excess β-CTF binds vacuolar ATPase, hobbling lysosomal acidification.
As massive, complex datasets burst onto the scene, scientists are using machine learning to analyze the data and uncover hidden patterns. AI may also come in handy in detecting dementia before humans do.
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