Helices at the end of TDP-43 help the protein condense into liquid droplets. ALS-associated mutations skew this liquid phase separation, promoting solid aggregates of TDP-43 instead.
The monoclonal antibody appears to remove plaques, although the small trial could not draw conclusions about cognition.
Different genetic factors underlie amyloid accumulation and atrophy, researchers at AAIC reported.
Edited by Michael Wolfe and authored by leaders in the AD field, a new book challenges investigators to make real progress.
Even as a slew of confounding variables blur results, studies still converge on the benefit of a cognitively stimulating life in old age.
Researchers at AAIC proposed several different measures of brain connectivity that may predict progression to AD.
A new PET ligand uncovers brain areas that are teeming with HDACs and other regions devoid of these enzymes.
Clinical trial design could benefit from new estimates of how slowly amyloid accumulates and how best to detect it at various disease stages.
While the relationship between Alzheimer’s and cardiovascular problems such as hypertension and diabetes remains complicated, a history of stroke is said to double the risk of late-onset AD.
In a validation study, three common software packages produced excessive false positives, but initial stories about previous suspect data might have been overblown.
BACE inhibitors are shaping up; pyroglutamate Aβ antibody clears plaques without ARIA, but immune reaction raises a flag.
Scientists report a way to stop transcription of the repeat expansion, leaving the normal gene alone.
Researchers at AAIC discussed technical limitations of current tracers and ways to improve the signal. A new ligand debuted that may be more specific for tangles.
Researchers at AAIC presented congruent data on the place tau tangles take in AD progression, and their close correlation with cognitive decline.
Profile matches Braak staging regions, suggesting those areas are particularly susceptible to AD pathology.