Months before mice develop plaques, faulty lysosomes swollen with Aβ commandeer plasma, ER, and Golgi membranes, creating toxic rosettes around the nucleus. The neurons eventually burst, leaving behind plaques.
Adeno-associated viruses carrying Cas9 and guide RNAs cut hexanucleotide repeats out of the C9ORF gene. RNA inclusions and poly-dipeptides became sparse.
A provocative new study suggests that unlike in mice, TSPO in people does not rise with microglial activation; instead, a higher PET signal reflects more microglia.
The first FDA approval of a CSF test, and increased options for plasma testing, will give patients easier access to these diagnostic aids. Will physicians interpret them properly?
A population of AGTR1-expressing dopaminergic neurons in the ventral slice of the human substantia nigra were selectively vulnerable in Parkinson's disease. These cells also expressed the most PD risk genes.
In wake of Medicare coverage decision, Biogen jettisons aducanumab sales staff but keeps trials going. Eisai/Biogen wrap up accelerated approval application to U.S. regulators.
One of the largest studies to date links sleep problems in middle age with worse cognition and lower brain volume years later. What causes what remains unclear.
Years before plaques develop in AD, the cingulate cortex brims with excess activity. Ditto in APP knock-in mice, where listless astrocytes allow a neuronal frenzy. Do astrocytes play into the pathological cascade this early?
In neurons lacking PS1, late endosomes get bogged down by imbalanced calcium. This puts kinases in a tizzy, slows motor proteins, and makes neurites dystrophic.
Depleted of cholesterol, neurons laid out the welcome mat for tau aggregates, which readily crossed into the cytosol and seeded aggregation there. Adding cholesterol blocked entry and seeding.