APOE Tied to Increased Susceptibility to SARS-CoV-2
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.
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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.
Two papers report that the ApoE4 allele triggers both hallmarks of AD in iPSC-derived cultures, in contrast to its minimal effects in mouse neurons.
A section of the protein folds on itself to form five layers. Three V-shaped layers cradle each other. This differs from the double-spiral fold in people with FTD/ALS.
DNA from leaky mitochondria unleash the cGAS-STING cascade, triggering interferon responses in the brain.
Researchers unearthed 75 risk loci, 42 of them new, and nominated candidate genes for each. A polygenic risk score based on all variants predicted AD risk with high accuracy.
DOPA decarboxylase in blood or CSF, and damaged mitochondrial DNA in blood cells, separated cases from controls.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Signaling within microglia requires dozens of substrates of γ-secretase. Without the enzyme, the cells barely react to plaques in mice.
A new study casts neuronal hyperexcitability as the link between Aβ aggregation in the neocortex and tau pathology in the medial temporal lobe.
In AD brain, microglia make less of the full-length protein. Loss of INPP5D releases the brakes on inflammation, and may spur microglial phagocytosis.
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