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.
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s pathology.
Levels of irisin are lower in brain and CSF of AD patients. Upping expression in mice protected them from synaptic deficits and memory problems.
Researchers characterize widespread cerebral amyloid angiopathy and cortical plaques found in three living people who received dural grafts as children.
In presynapses, binding sequesters synaptic vesicles.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
First look at substrate interactions reveals similarities but some surprises.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.