A novel assay detected two strains of human SOD1 in mice expressing the protein. They differed from those that formed in vitro. Researchers hope to use the technique to identify strains of other problem proteins as well.
Approximately 4 percent of familial ALS cases may be due to TBK1 mutations.
Sequences of more than 2,600 Icelanders link loss-of-function mutations in the ABCA7 gene to increased risk for Alzheimer’s.
Antibody against aggregated Aβ reported to clear out amyloid from brain, and perhaps slow cognitive decline, in people with prodromal Alzheimer’s disease.
Researchers found inherited recessive or dominant de novo mutations in people with sporadic ALS whose parents did not have the disease.
Motor neurons may be susceptible to ALS because they lack a chaperone that folds SOD1.
Phase 2 trial data show promise, say researchers.
Cognitively normal people with levels of CSF Aβ42 near the cutoff point associated with amyloid pathology are likely to cross that threshold within three years.
The British government, pharmaceutical companies, and a research charity establish a venture capital fund.
A chloride ion imbalance renders γ-aminobutyric acid (GABA) receptors excitatory.
Researchers at a Keystone meeting reported that a combination of protective and destructive signals target microglia to prune synapses in the brain. These signals may be altered during disease.
Similar regulators could be the next frontier in neurodegeneration studies, scientists say.
The ALS- and FTD-linked expansion, once it reaches more than 90 repeats, always manifests methyl groups.
Risk alleles of SORL1 dampen its expression in response to growth factors, leading to higher Aβ production.
When ultrasound opens the blood-brain barrier in mice, microglia engulf plaques.