Neuronal markers in the cerebrospinal fluid suggest the degree of white-matter damage correlates with time needed for recovery, and that repetitive brain injury spurs amyloid deposition.
With a laser focus on biomarkers and disease mechanisms, researchers at the 10th ICFTD meeting prepared the ground for therapeutic studies.
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.
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?
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.
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