With Age, Microglia Pump cGAS, Revving Harmful Inflammation
DNA from leaky mitochondria unleash the cGAS-STING cascade, triggering interferon responses in the brain.
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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.
The patient, an APOE4 homozygote with severe cerebral amyloid angiopathy, developed vascular inflammation and bleeding throughout her brain.
Growth-associated protein 43 in the CSF identified people who accumulated tangles fastest. These spread through connected brain regions.
In CD8+ T cells and monocytes, DNA was more accessible in people with AD and even more so in ApoE4 carriers.
ApoE2 reported as raising risk for progressive supranuclear palsy, a rare tauopathy.
The decade-long trial found no benefit for solanezumab in delaying progression, but laid the groundwork for subsequent prevention studies.
Topline results showed no statistically significant slowing of decline on either of two primary endpoints. Trends across multiple endpoints favored crenezumab.
Biogen researchers claim the antibody worked in people who got enough of it. To other researchers, the signal validates the amyloid hypothesis and injects fresh energy into the field. But is this interrupted dataset enough to approve?
An interim analysis predicted the antibody would not slow Alzheimer’s progression; a crenezumab trial in autosomal-dominant AD is continuing.