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.
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?
Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
Clusters of neurons harboring somatic mutations in 56 genes linked to neurodegenerative diseases may be commonplace in the human brain.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s pathology.