Striking Microgliosis in New APP Knock-in Mice
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
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Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
Whole-genome sequencing combined with expression data identifies five LBD loci: three known and two new. Four increased LBD risk while one appears protective.
Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
This neuronal protein regulates the complement cascade in the developing brain. Could it do the same in aging or neurodegenerative disease?
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
Without the WD domain of Atg16L1, required for a newly discovered type of endocytosis, old mice develop hallmark pathologies of AD.
In the mouse retina, these tender threads connect pericytes on nearby capillaries. They enable cells to coordinate constriction and dilation of blood vessels in response to neuronal activity.
Dendritic tau suppresses production of nitric oxide, which prevents blood vessels from dilating in response to neural activity.
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
Three studies agree that TMEM106b/progranulin double knockouts develop more extreme lysosomal dysfunction, inflammation, and motor deficits than PGRN KOs.
TRP cation channels combine with extrasynaptic NMDA glutamate receptors to set off mitochondrial meltdown and cell death. Blocking the interaction stops excitotoxicity.
ApoE4 does so much more strongly than the other known genes collected in a polygenic risk score.
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
Despite overall falling dementia rates in the U.S., black people remain more susceptible than whites.