Homing in on Early Alzheimer’s Biomarkers: Does Connectivity Hold the Key?
Researchers at AAIC proposed several different measures of brain connectivity that may predict progression to AD.
6400 RESULTS
Sort By:
Researchers at AAIC proposed several different measures of brain connectivity that may predict progression to AD.
Even as a slew of confounding variables blur results, studies still converge on the benefit of a cognitively stimulating life in old age.
Edited by Michael Wolfe and authored by leaders in the AD field, a new book challenges investigators to make real progress.
Different genetic factors underlie amyloid accumulation and atrophy, researchers at AAIC reported.
The monoclonal antibody appears to remove plaques, although the small trial could not draw conclusions about cognition.
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.
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.
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.
Read our full coverage of this year’s AAIC conference.
Parabiosis passes its first test in mouse models of Alzheimer’s, normalizing gene expression and improving memory—though with no reduction in amyloid plaques.
Researchers explain why the protease cuts at every third amino acid, shedding light on how some familial APP mutations are pathogenic.
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.
P25 overexpression in APP transgenic mice is one of perhaps many artifacts of APP overexpression, APP, researchers charge. Do APP/PS1 transgenic mouse phenotypes need re-evaluation?
Researchers report that tau accumulation in the cortex associates with cognitive impairment in people with ongoing synucleinopathy. Aβ is not necessary for this type of tauopathy.
With a laser focus on biomarkers and disease mechanisms, researchers at the 10th ICFTD meeting prepared the ground for therapeutic studies.
No filters selected