In mice, disease-associated microglia proliferate so much that they become senescent. Plaques then run amok and synapse are lost.
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.
In the face of aging or amyloidosis, microglia lacking C9ORF72 ramped up interferon genes, accumulated lysosomes, and ate synapses.
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.
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.
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.
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.
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.
When pulsed through the skull, ultrasound restored synaptic signaling, neurogenesis, and memory, in old mice.
Activating the G protein-coupled receptor PAC1R in the mouse brain prompts the proteasome to clear tangles.
Unlike iPSC-derived neurons, those created directly from fibroblasts reflect the donor's age and disease status. Epigenetic modifications appear to make the difference.
In the plaque-ridden mouse brain, microglia that had taken up Aβ activated a unique gene-expression profile. It faded after microglia were moved to plaque-free environs.
A person's blood phospho-tau level, combined with his or her APOE genotype and scores on executive function and memory tests, outperforms the clinician in predicting dementia within the next four years.
Downregulation of a chemokine receptor traps T cells in the meninges. Glymph drainage slows, amyloid burden rises.
A “mammalian-wide interspersed repeat-natural antisense transcript” blocks translation of tau mRNA. Other MIR-NATS may act on α-synuclein and APP.