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.
A new prize seeks the ideal mix of factors to forecast who will progress to Alzheimer’s symptoms.
23andMe sells people information about their Alzheimer’s and Parkinson’s risk. They include tricky-to-interpret raw data on dozens of disease genes. Should such direct-to-consumer testing companies offer better counselling and referral?
Instead of clearing plaques, do microglia seed them? The brain’s immune cells continue to take researchers by surprise.
Microglial Regulation and Function Scrutinized at Heidelberg Meeting A New Explanation for Dendritic Tau: It’s Made There Alzheimer’s Proteomics Treasure Trove? sAPP Binds GABA Receptor, and More News on APP At Heidelberg meeting, scientists shared and ...
The first high-resolution structures of tau filaments isolated directly from an Alzheimer’s brain lay bare C-shaped protofilaments with a surprising twist.
Microglia lacking TDP-43 efficiently remove Aβ. In the process, they go a little crazy and also attack and destroy synapses.