Could an RNA-Binding Protein Prevent Tau Aggregation?
When human neurons and brain organoids lack G3BP2, they contain more tau oligomers. The protein binds to tau’s microtubule-binding domain.
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When human neurons and brain organoids lack G3BP2, they contain more tau oligomers. The protein binds to tau’s microtubule-binding domain.
α-Synuclein seed amplification assays identify people with LBD. They may outperform clinical diagnosis, and hint that dementia with Lewy bodies might be overdiagnosed.
In mice, microglia that sprout vascular cell adhesion molecule 1 flock to amyloid aggregates. ApoE is required.
Raising TMEM164 prevents astrocytes from releasing the toxic lipids, protecting neurons in models of Alzheimer’s and Parkinson’s.
The second-generation PET ligand snuggles into the C-shaped protofilaments of tau fibrils extracted from an AD brain sample.
In human three-dimensional brain cell cultures, UBB+1 caused plaques and tangles. Silencing UBB+1 prevented spontaneous amyloid pathology caused by AD mutations.
In contrast to phospho-tau species that mirror amyloid, CSF MTBR-tau-243 reflects tau-PET. It fell upon treatment with an antibody against tau’s midsection.
An antibody copying the effects of the protective ApoE variant prevents tau hyperphosphorylation in the mouse eye and brain.
These imaging abnormalities grew the most in people with many plaques or cerebral amyloid angiopathy pathology, irrespective of cardiovascular risk.
In a Phase 1 trial of Roche’s RG6289, both plasma and CSF Aβ37 climbed, while Aβ42 fell.
In mice with amyloidosis, removal of miR-155 from microglia rendered the cells more receptive to IFN-γ stimulation, improving neuroprotection.
A comparative snRNA-Seq study of three regions from AD, PSP, and FTD brains identifies subtypes of neurons and glia hit hard in each disorder.
Whether expressing two copies of APOE3 or -E4 with this variant, mice had less tauopathy, gliosis, atrophy. One copy of Christchurch partially protected.
Twelve people heterozygous for this protective variant were still sharp seven years after their expected age of AD onset. One had fewer tangles than expected.
Each associates with distinct AD risk variants, brain atrophy, and disease severity.