Markers of necroptosis peppered postmortem brain tissue from people with AD. Gene expression implicates RIP kinases. Could shuttering this cell death pathway save neurons?
Finally, a Blood Test for Alzheimer’s? What went down in London town during the AAIC meeting? Whether you were there or could not go this year, Alzforum reporters captured the highlights. Read about a promising plasma Aβ assay that flags people who have ...
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.
Gaps surrounding blood vessels in the brain may predict cognitive decline and vascular dementia.
The updated, expanded manual helps doctors diagnose this rare tauopathy and its variants earlier, in hopes that more patients can take advantage of clinical trials.
The prevalence of chronic traumatic encephalopathy supports a link between multiple concussions and this degenerative tauopathy, though the sample is self-selected.
An astrocytic Aβ protease, destabilization of γ-secretase by FAD mutations, and an sAPP receptor all made their debuts at Heidelberg conference.
Run-on repeats not only break DNA, they thwart the crucial repair pathways needed to sew the strands back together.
Knockout mice suggest opposing effects on lysosomal enzymes and neurodegeneration in frontotemporal dementia, implicating an ATPase.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
Researchers identified nuclear protein SRSF1 as the culprit that allows aberrant C9ORF72 RNA to escape into cytoplasm and give rise to toxic dipeptide repeat proteins.
Tau takes its place among the growing cadre of neurodegenerative disease proteins known to form liquid droplets. How the protein’s liquid form relates to its toxicity remains unclear.
Transcriptional profiling of human microglia sheds light on species differences, raising caution about translatability of rodent studies.
At a conference in Heidelberg, researchers proposed that Aβ oligomers trigger local translation of tau in cytosol and dendrites, and that targeting this aberrant tau may preserve synapses.
An antibody that activates Notch 3 signaling helps keep retinal blood vessels intact in a mouse model of the small vessel disease CADASIL.