Roche and Prothena publish Phase 1b results for their antibody PRX002/RG7935.
Tiny yet mighty, small carbon structures glom onto and dissolve α-synuclein fibrils, neutralizing their toxicity in mouse models of Parkinson’s disease.
Researchers found large deletions, inversions, or insertions in about one-fifth of edited cells, suggesting caution for therapeutic uses of the technology.
By loosening their chromatin straitjackets, and reining in their RNA watchdogs, tau unleashes transposable elements into the genome.
The microfluidic device could test the vascular contributions to neurodegenerative disease and bioavailability of drugs for the brain.
A new PET tracer belies previous results from animal models and postmortem studies. Caveat emptor for trials of HDAC inhibitors?
Translatome profiling suggests ApoE drives a microglial gene-expression signature found in aging, Aβ amyloidosis, and tauopathy.
By yanking a nuclear protein out of its pore, phosphorylated tau makes nuclei leaky, disrupting the strictly controlled passage of proteins and setting tau up for aggregation.
In large cohorts, older people tested in summer and autumn scored higher on cognitive tests than people tested in winter and spring. Is a seasonal clock ticking in the background?
Serial data establishes different trajectories for CSF t-tau and p-tau.
Families of ALS and FTD patients with C9ORF72 expansions have more mental illness, suggesting the gene affects brain function throughout life.
In a fly model of neurodegeneration, CDK5 slams autophagy, which leads to a runaway immune response that shoves aging neurons over the edge.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
Regulatory T cells rush into the brain after a stroke, quelling astrocytosis and aiding neural recovery.