Idalopirdine failed to slow memory decline in patients with Alzheimer’s disease.
Sometimes challenged, the idea that pathogenic proteins spread through the brain got a lift from new animal model data presented at the frontotemporal dementia meeting.
Geneticists at frontotemporal dementia conference reported a new link with a ubiquitine enzyme and strengthened other gene associations.
Several such tests generated enthusiasm at the international frontotemporal dementia congress.
Researchers at an international frontotemporal dementia congress reported progress in finding markers that track disease, but no luck thus far with diagnostic markers.
Researchers reported negative findings from three trials at ICFTD 2016.
Frontotemporal Dementia: The Hard Work of Pushing Toward Trials First Round of FTD Therapeutics Fell Short, But Many More Are Up and Running Fluid NfL Shines, Tau PET Dims, in the Hunt for FTD Biomarkers Tests of Social Cognition Hold Potential as FTD ...
ApoE2 enhances, while ApoE4 reduces, astrocytes’ ability to gobble up synapses. Researchers propose this is one way the apolipoprotein modulates AD risk.
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.