TWAS x GWAS? Transcriptome Analysis Finds 11 Parkinson’s Genes
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
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Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Researchers envision p-tau-based blood tests for Alzheimer’s disease within a few years, but maybe not a stand-alone test.
New research implicates IL-6 signaling and even Aβ42 itself as BACE targets, complicating efforts to resurrect BACE inhibitors at a low dose.
After news on “new data” they won’t see, three committee members argue against approval.
In mice, polyamines boost autophagy and promote clearance of soluble Aβ species. In cells, they counteract tau aggregation. In the Alzheimer’s brain, their metabolism is ramped up. Could spermidine supplements prevent or treat AD?
When pulsed through the skull, ultrasound restored synaptic signaling, neurogenesis, and memory, in old mice.
The anti-tau immunotherapy did not slow cognitive decline among people in the earliest stages of AD, nor did it evoke changes on tau-PET scans.
Alector’s AL002c antibody mobilizes microglia, reduces neuronal dystrophy, and restores normal behavior—all in mice. The clinical version is in Phase 1.
The transcription factor NFATc2 mediates this response.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
Incorporation of a cryptic exon scuttles translation of UNC13A, but only in neurons lacking nuclear TDP-43. UNC13A ALS/FTD risk variants exacerbate the aberrant splicing.
Islet amyloid protein and Aβ fibrils share similar folds.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.