Finally, a Blood Test for Alzheimer’s? In Clinical Use, Amyloid Scans Change Two-Thirds of Treatment Plans Searching for New AD Risk Variants? Move Beyond GWAS Monomeric Seeds and Oligomeric Clouds—Proteopathy News from AAIC Planning the First Primary Pre
Markers of necroptosis peppered postmortem brain tissue from people with AD. Gene expression implicates RIP kinases. Could shuttering this cell death pathway save neurons?
One report implicates APP’s intracellular domain in neuron loss due to LRRK2; another accuses the AICD fragment of regulating mitochondrial dynamics via Pink-1.
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.
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.
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.
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.
At AAIC 2017, 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.
Rather than changing one by one, many biomarkers—including cognition, tau PET, hippocampal atrophy, and CSF p-tau—shift together, around the time of symptom onset in young adults with familial AD.