AAV-based CRISPR snipped a piece of mutant APP and limited plaques in mice. Viruses that infiltrate only the CNS—and only neurons there—may facilitate localized gene editing in the brain.
Without TREM2, microglia remained trapped in a homeostatic state and failed to clear TDP-43 aggregates. In a surprising twist, the two proteins were found to interact.
Tissues from old people, both healthy and diseased, overexpress genes lacking C-G repeats. This stokes inflammation, possibly explaining why neurodegeneration rises with age.
The EMA's decision was expected. Biogen announced it will appeal but also halved the drug's price. The company said it plans to complete a confirmatory trial by 2026.
For amyloidogenic proteins such as Aβ and tau, third-party proteins bearing similar sequences sway aggregation kinetics. Does this underlie cells’ selective vulnerability to amyloid?
A repurposing study tapped sildenafil as an Alzheimer’s drug candidate. It suppresses p-tau in cultured neurons, men who take it are less prone to AD, and a trial is planned.
Cryo-EM revealed that TDP-43 protofilaments from people with ALS/FTD formed the same structure, with a core of stacked double spirals. It is wildly different from that of TDP-43 filaments made in vitro, and from those of other amyloids.
Blood from fit mice reduced neuroinflammation in inactive mice. The can-do component? Clusterin, an apolipoprotein linked to Alzheimer’s. Clusterin tamped down interferon and cytokine signaling.
At CTAD, scientists presented an electronic version of the CDR, plus new digital tests. Will smartphone apps pick up mild cognitive impairment and even preclinical cognitive change?
In human microglia-like cells, soluble CD22 stalled normal breakdown of fats. Blocking sCD22 greased the system, evoking a treatment for lysosomal-storage disorders.