At AAIC2017, scientists offered new clues on sleep and AD neuropathology. They identified parts of the brain that may be involved and highlighted the benefits of treating sleep disorders.
Motor symptoms slightly improved in 31 patients taking exenatide for 48 weeks, while the placebo group worsened. The effect persisted three months after treatment stopped.
Injecting a piece of this anti-aging protein days before memory testing improved performance in mice young and old, as well as those that overexpress α-synuclein.
High-throughput sequencing yields surprises. Learn about pathogenic variants in endosomal genes, an algorithm to nab the worst SORL1 mutations, dominant PS1 mutations arising de novo, and tau duplications.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
Report details ways to improve care of people who have dementia, argues for societies to implement ambitious prevention strategies, but offers only reduction of hypertension as a plausible intervention.
Scientists at AAIC described a large, multidomain intervention trial in the United States to test if lifestyle changes can stave off cognitive decline. YMCAs nationwide are in on the project; similar trials are in the works in other countries.
TREM2 knockout causes a metabolic meltdown in microglia, but treating mice with cyclocreatine restores ATP levels and rejuvenates the cells to fight amyloid.
Findings from a 25-year longitudinal study in a large, biracial cohort point to preventable mid-life vascular problems as a top dementia risk factor.
FUS proteins tend to link up and form liquid droplets and, from those, aggregates. Phosphorylation of the protein’s low-complexity domain repels these associations.
Researchers will enroll young adults who carry familial AD mutations in the first trial of a mechanism-based, investigational drug to try to prevent amyloid from depositing in the brain.
In London, researchers claimed that a monomer is the minimal structure required for tau strains. On the other hand, the sky seems the limit for the number of Aβ strains that form in an individual brain.
At AAIC 2017, researchers presented new approaches to find genetic variants linked to AD risk and to understand their contributions to disease.
CRISPR-Cas9 gene editing rids embryos of a mutation causing heart disease, evoking a future where autosomal-dominant disease is prevented at the DNA level. What about AD, FTD, and ALS?