Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
An interim analysis predicted the antibody would not slow Alzheimer’s progression; a crenezumab trial in autosomal-dominant AD is continuing.
Reducing systolic blood pressure staves off cognitive decline, but what about dementia?
A periodontal pathogen found in human brains triggers AD pathology in mice. Will an antibiotic stave off dementia?
Frail people may be more likely to have Aβ plaques and neurofibrillary tangles; when they do, they are more likely to have dementia. Physical activity correlated with better global cognition, regardless of brain pathology.
Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
Ever wonder why it’s so easy to nod off in a hammock? Turns out swaying back and forth improves sleep and even enhances memory in people.
Are high-molecular-weight, multi-protease complexes cellular Aβ factories?
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
In neurons derived from FTD patients, microtubules distort the nucleus, warping its normally rounded membrane and disrupting communication with the cytoplasm.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.
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.