When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
In a tiny pilot trial, people with amyotrophic lateral sclerosis who took a “cellular health and optimization” supplement were reported to have improved on several clinical outcome measures.
An interim analysis predicted the antibody would not slow Alzheimer’s progression; a crenezumab trial in autosomal-dominant AD is continuing.
A newly uncovered population of astrocytes in layer V of the cortex modulate synapses by secreting a protein linked to Norrie disease, a form of blindness. Are other disease-related astroglia lurking in the brain?
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
A periodontal pathogen found in human brains triggers AD pathology in mice. Will an antibiotic stave off dementia?
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
DAPPD suppressed neuroinflammation and preserved cognition in mouse models of amyloidosis, suggesting potential for treating Alzheimer’s disease.
In a mouse tauopathy model, knocking out the NLRP3 inflammasome prevented toxic tau from forming.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Biogen researchers claim the antibody worked in people who got enough of it. To other researchers, the signal validates the amyloid hypothesis and injects fresh energy into the field. But is this interrupted dataset enough to approve?
Aberrant gene-expression patterns found to be common to human neurodegenerative disease and animal models. MicroRNA and epigenetic modification may be to blame.
Boosting sTREM2 in the brain rallied microglia to clear Aβ plaques, restored synaptic plasticity, and even rescued memory deficits in mice.