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.
A risk allele previously linked to Parkinson’s is now extended to Alzheimer’s as well, with particularly strong effects in patients who lack an ApoE4 allele.
In mice lacking BACE1, fewer potassium ions escape hippocampal neurons, causing brain cells to fire more rapidly.
Mice expressing presenilin harboring AD-associated mutations resemble mice lacking the enzyme altogether, suggesting that the mutations fully inactivate the enzyme.
The brain’s resident immune cells secrete galectin-3, which activates other nearby microglia to promote neuroinflammation.