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.
A U.S. study claims that proton pump inhibitors commonly used to treat acid reflux are not associated with an increased risk of dementia, countering a recent German study.
Biopsies from kids with stomach distress reveal nerve cells that release α-synuclein during infection.
In older carriers of the Alzheimer’s risk allele, certain brain regions fail to adapt to increasing task difficulty.
Aberrant proteins made in C9ORF72 cells disrupt splicing by binding U2 snRNP, a key component of the spliceosome.
Researchers combine seven factors to predict if PD patients will become demented in the decade after diagnosis.
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