Does Neural Activity Drive DNA Repair?
In mice, the neuronal transcription factor NPAS4 recruits DNA repair machinery to active promoters; without it, double-strand DNA breaks accumulate.
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In mice, the neuronal transcription factor NPAS4 recruits DNA repair machinery to active promoters; without it, double-strand DNA breaks accumulate.
A single injection with CRISPR machinery suppressed mutant protein and improved gait and survival, suggesting the strategy deserves further exploration.
The fatty acid shields Syt11 from degradation. With more of it around, α-synuclein monomers cling to membranes.
Meaningfulness must account for the disease stage a patient is at, his or her priorities, and effects over time, researchers say.
Scientists turned iPSCs from people with ALS or Parkinson’s into motor neurons or dopaminergic neurons, respectively, then characterized them with a plethora of multi-omics.
Cognitively normal older adults with high levels of the biomarker slid quickly toward dementia.
Can joint analysis of gene expression, chromatin, and transcription factors help explain how transcription changes in Alzheimer’s disease?
In mice, oligomeric Aβ causes these macrophages to produce SPP1. Knocking out this pro-inflammatory cytokine quiets microglia and protects synapses.
As it moves from the neutral pH of the cell surface to the acidic environs of the endosome, LRP2 switches its conformation from ligand receiver to dumper.
Microglia within 10 micrometers of Aβ plaques expressed a disease-associated signature. Astrocytes rubbernecked from a bit farther away.
Mis-splicing events produce novel proteins that can be detected in the cerebrospinal fluid of ALS/FTD patients before their symptoms start.
The protein binds to segments of tau that are prone to aggregate, preventing tangles and neurodegeneration.
Twelve severe viral illnesses boosted risk up to 15 years after infection.
SORL1 may form polymers that bind and stabilize the retromer, facilitating the recycling of APP and other substrates.
p-S129syn better binds its synaptic vesicle protein partners than does plain α-synuclein.
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