At CTAD, all eyes were on the anti-amyloid antibody donanemab, which is before the FDA. Scientists showed how Phase 3 is enrolling, and how plasma tau enables wholly remote inclusion of people with plaques and tangles.
As it moves from the neutral pH of the cell surface to the acidic environs of the endosome, LRP2 switches its conformation from ligand receiver to dumper.
Adeno-associated viruses carrying Cas9 and guide RNAs cut hexanucleotide repeats out of the C9ORF gene. RNA inclusions and poly-dipeptides became sparse.
In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
Scientists turned iPSCs from people with ALS or Parkinson’s into motor neurons or dopaminergic neurons, respectively, then characterized them with a plethora of multi-omics.
The p-tau217/tau217 ratio in the cerebrospinal fluid tightly correlated with amyloid, while p-tau205/tau205 best detected neurofibrillary tangles and neurodegeneration.