Newly ensconced at the National Institute on Aging’s Division of Neuroscience, Masliah urges researchers to participate “at all levels” in the community-driven process to implement the national plan. His lure? Finally, more money.
Researchers explain why the protease cuts at every third amino acid, shedding light on how some familial APP mutations are pathogenic.
New evidence suggests that Aβ trimers cause tau to misfold, then together, the soluble miscreants gum up axonal transport.
Parabiosis passes its first test in mouse models of Alzheimer’s, normalizing gene expression and improving memory—though with no reduction in amyloid plaques.
Read our full coverage of this year’s AAIC conference.
AD-linked mutations in presenilin 1 increase the enzyme’s cleavage of STIM1a endoplasmic reticulum calcium receptor, reducing Ca2+ influx into neurons and destabilizing dendritic spines. Researchers proposed targeting the pathway as a therapy.
Increasingly, people must learn of their amyloid status and/or ApoE genotype in order to enter secondary prevention trials. At AAIC, researchers laid out their procedures to ethically break the news.
Children lacking a gene needed for clearing away tired mitochondria develop a rare neurodegenerative disorder.
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.
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