Risk alleles of SORL1 dampen its expression in response to growth factors, leading to higher Aβ production.
The ALS- and FTD-linked expansion, once it reaches more than 90 repeats, always manifests methyl groups.
Similar regulators could be the next frontier in neurodegeneration studies, scientists say.
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.
A chloride ion imbalance renders γ-aminobutyric acid (GABA) receptors excitatory.
The British government, pharmaceutical companies, and a research charity establish a venture capital fund.
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.
Phase 2 trial data show promise, say researchers.
Motor neurons may be susceptible to ALS because they lack a chaperone that folds SOD1.
Researchers found inherited recessive or dominant de novo mutations in people with sporadic ALS whose parents did not have the disease.
Approximately 4 percent of familial ALS cases may be due to TBK1 mutations.
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.
Microbleeds in the brain portend either stroke or cardiovascular events, depending on where they occur.
Treatments targeting the main pathological protein of Parkinson’s disease are moving toward the clinic, with two immunotherapies passing Phase 1 safety benchmarks.
The newest contender in the race for a drug to rein in the β-secretase enzyme debuted with data that reflected a methodical approach to understand a drug’s performance in cerebrospinal fluid before looking for efficacy.
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