Downregulation of a chemokine receptor traps T cells in the meninges. Glymph drainage slows, amyloid burden rises.
After news on “new data” they won’t see, three committee members argue against approval.
Herpes infection upped risk in ApoE4 carriers, damaged brain tissue, and correlated with neurodegeneration markers in the CSF.
Via recently discovered channels, freshly made monocytes and B cells in the bone marrow of the skull and vertebrae travel directly into the meninges, where they stand ready to infiltrate the brain. These immune cells are distinct from their blood-borne counterparts.
A set of 19 plasma proteins identified clinical Alzheimer’s cases with 97 percent accuracy, and it distinguished mild versus severe dementia. The panel was tested in two small cohorts.
The anti-tau immunotherapy did not slow cognitive decline among people in the earliest stages of AD, nor did it evoke changes on tau-PET scans.
The L1CAM cell adhesion marker is a widely adopted marker of neuron-derived extracellular vesicles. Except it cannot be found in those teeny packets, claims a new study.
In mice, disease-associated microglia proliferate so much that they become senescent. Plaques then run amok and synapses are lost.
The tau vaccine evoked a robust anti-tau antibody response, which curbed the rise in plasma NfL and CSF p-tau over two years. Cognitive decline continued.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
The Phase 2 trial provides the strongest evidence yet that removing most amyloid from the brain bolsters cognition, although the benefit is small.
In the face of aging or amyloidosis, microglia lacking C9ORF72 ramped up interferon genes, accumulated lysosomes, and ate synapses.
Certain neurons crank up ApoE expression with age in mice. Ditto with AD progression in people. These same neurons ramp up immune response genes. The shift could foreshadow their demise.
Biogen got the go-ahead under the FDA’s accelerated approval pathway, which requires change in a surrogate biomarker and Phase 4 studies to verify a clinical benefit.
A large multinational epidemiology study finds only small and inconsistent associations.