Mutations that destabilize α-synuclein tetramers leave young mice with severe and progressive motor problems resembling those of PD.
Believed to be an amyloid-lowering agent, the blood pressure drug did not help people at the dementia stage of disease.
In a new take on mosaicism and Alzheimer’s, scientists claim that APP mRNAs convert into DNA and reinsert into the genome. Full of mutations, these “genomic cDNAs” crop up in aging and sporadic AD.
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.
A periodontal pathogen found in human brains triggers AD pathology in mice. Will an antibiotic stave off dementia?
The 2019 budget ups this year’s spending by $425 million.
A behavioral intervention slowed memory slippage and functional decline over two years.
A molecular-level view of tau filaments from a person with Pick’s disease reveals that the protein folds up differently than it does in Alzheimer’s disease.