Researchers characterize widespread cerebral amyloid angiopathy and cortical plaques found in three living people who received dural grafts as children.
Levels of irisin are lower in brain and CSF of AD patients. Upping expression in mice protected them from synaptic deficits and memory problems.
When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
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.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
A periodontal pathogen found in human brains triggers AD pathology in mice. Will an antibiotic stave off dementia?
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
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.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
Two independent studies find that loss of nuclear TDP-43 leads to mis-splicing of stathmin 2, an essential protein for axon growth and repair.